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INTERNATIONALE PHARMACEUTICA SCIENCIA

| Jan-March 2011 | Vol. 1 | Issue 1 |


Available online http://www.ipharmsciencia.com
2011 IPS
REVIEW ARTICLE

A Review of Phytochemistry and Pharmacology of Flavonoids


Harleen Kaur Sandhar, Bimlesh
Kumar*, Sunil Prasher, Prashant
Tiwari, Manoj Salhan, Pardeep
Sharma

ABSTRACT
Flavonoids are natural products widely distributed in plant kingdom and currently
consumed in large amounts in the daily diet. These are categorised according to

Lovely School of Pharmaceutical


Sciences, Lovely Professional
University, Jalandhar-Delhi G.T. Road
(NH-1), Phagwara. Punjab (INDIA)
144402

their molecular structures into flavonols, flavones, flavanones, isoflavone, Catechin,


anthocyanidin and chalcones. Flavonoids are capable of modulating the activity of
enzymes and affect the behaviour of many cell systems and exerting beneficial
effects on body. This property of flavonoids has aroused considerable interest. This

Date of Submission: 22-01-2011


Date of Acceptance: 14-03-2011
Conflict of interest: Nil
Source of support: None

review has presented the recent research advancements of chemistry and


pharmacological properties of flavonoids.
Key words: Flavonoids, Quercetin, Rutin, Apigenin, Flavone, Chalcone,
Kaempferol, Antioxidant, radical-scavengers

On the basis of C-skelton, polyphenols are classified as:

INTRODUCTION
Phytochemicals are defined as the substances found in

1.

Flavonoids

edible fruits and vegetables that exhibit a potential for

2. Phenolic acids [2]

modulating human metabolism in a manner beneficial


for the prevention of chronic and degenerative diseases

FLAVONOIDS

[1].

Flavonoids are low molecular weight

Phenolics are defined as a class of polyphenols which

polyphenols[9]

are important secondary metabolites present in plants

photosynthesising cells[10]. The original "flavonoid"

and are also responsible for their antioxidant action

research apparently began in 1936, when Hungarian

and various beneficial effects in a multitude of diseases

scientist Albert Szent-Gyorgi was uncovering a synergy

[3, 4].Polyphenols

between pure vitamin C and as yet unidentified co-

[2]

are characterised as :

1. Phenolic compounds: Are aromatic organic

play

vital

bioactive
role

in

factors from the peels of lemons, which he first called

compounds with at least one hydroxyl group

"citrin," and, later, "vitamin P" [11].

attached directly to a benzene ring. These are

Flavonoids are secondary metabolites characterised by

hydroxylated derivatives of benzoic acid, present

flavan nucleus

in form of esters and glycosides.

These are group of structurally related compounds

2. Phenolic acids: cinnamic acid derivatives. Often


present in esterified form.
3. Glycosidic phenylpropanoid esters [5,6].

with

[8]

and C6-C8-C6 carbon-skeleton

chromane-type

skelton

having

[12, 13].

phenyl

substituent in C2-C3 position

[14].

feature

2-phenyl-benzo--pyrane

of

flavonoid

is

The basic structural

nucleus consisting of two benzene rings (A and B)

Address for correspondence


*Bimlesh Kumar (Lecturer)
Dept. of Pharmaceutical Sciences, Lovely Professional
University, Ludhiana-Jalandhar G.T. Road, Phagwara
(Punjab), 144402, India
*Mob: +919872260354, +919216260354
E.mail: bimlesh.12474@lpu.co.in, bimlesh1@gmail.com
25

which

[7, 8]

linked through a heterocyclic pyran ring (C) as shown


in fig (I) [10].

Internationale Pharmaceutica Sciencia

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Vol 1 Issue 1

Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids


3'

8
7

1'

groups bound to Carbon of aglycone usually 6-C or 8-C

4'

2'

[14].

5'

Optical activity of flavonoids:

6'

The flavonoids are a class of natural product that gains

interest due its great variety and the number of its

Fig (I): Basic structure of flavonoids [10]

members. The flavonoids are often hydroxylated in


positions 3, 5, 7, 3, 4, and 5 as shown in fig (IV)
which are frequently methylated, acetylated, or

Biosynthesis of Flavonoids:

sulphated.

O
S-CoA

H2C CH3
CH2

3CH3COOH

3'

2'

4'

O
O

HO

OH

OH

6'

5'

Fig (IV): Numbering of atoms in flavonoid aglycone


]
at which substitution may occur [15

Fig (II): Biosynthesis of flavonoids


Flavonoids differ in their arrangement of hydroxyl,
methoxy and glycosidic side groups and in the
conjunction between A and B rings [8]. A variation in C
[13].

1'

FLAVAN NUCLEUS

ring provides division of subclasses

According to

their molecular structure, they are divided into eight


(fig III) classes [13]:

The actual number of flavonoids that have been found


so far and for which the structure has been completely
elucidated is large, but probably does not exceed 1% of
the theoretical number of possible variants. This
abundance of variants is further augmented by the
chirality of the subunits and their connections. Since
many stereoisomers do not differ significantly in their
electronic or fluorescence spectra so the optical activity

O
O
O

of the species is often a useful analytical parameter [16].

H
H
O

OH

(1) Flavone

(2) Flavonones

(3)Flavonol

(4) Isoflavone

Distribution of flavonoids:
Flavonoids are widely distributed among the plant

3
2
3'

O+

4'

OH

H
H

OH

2'

nuts, seeds, stem, flowers, tea, wine etc. These are an

5'
6'

OH

kingdom [10].Flavonoids are found in vegetables, fruits,

4
B

(5) Anthocyanidin (6) Catechin (7) Dihydroflavonol (8) Chalcone

Fig (III): Chemical structure of different


types of flavonoids [15]
In plants, flavonoids are often present as O-glycosides
or C-glycosides. The O-glycosides possess sugar

integral part of our daily diet

[15, 17, 18].

The dietary

intake of flavonoids is estimated to be 1-2 g/day [7]. The


average intake of flavonols and flavones was found to
be 23 mg/day, among which, flavonol quercetin
contributed 16 mg/day

[8].The

table below (Table 1)

describes various flavonoids present in our daily


dietary food sources:

substituent bound to OH of aglycone, usually at


position 3 or 7, whereas, C-glycosides possess sugar

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

Table 1: Occurence of flavonoids in food [9, 19]:


S.
No.

Flavonoid
subclass

Food source

Representative
flavonoids

1.

Flavonol

Onion, kale, broccoli


apples, cherries,
berries, tea, red
wine

Kaempherol,
myricetin, quercetin,
rutin

2.

Flavones

Parsley, Thyme

3.

Flavonones

Citrus

4.

Catechins

Apple, tea

5.

Anthocyanidins

6.

Isoflavones

Cherries, Grapes
Soya beans,
Legumes

Apigenin, chrysin,
luteolin
Hesperitin, erodictyol,
naringen
Catechin,
galocatechin
---------------Daidzen, genistein,
glyciten, formanantine

Functions of Flavonoids in plants:


Anthocyanin pigment present in flowers provide colour
to it contributing to pollination

[8, 10, 20].

Flavonoids

present in leaves promote physiological survival of


plant by protecting it from fungal infections and UV
radiations. In addition, flavonoids are involved in
photosensitisation, energy transfer, respiration and
photosynthesis

control,

determination, energy transfer

morphogenesis,

sex-

[10].

Indian Plants containing Flavonoids:


Table 2: Medicinal plants found in India and rich in flavonoids content
S.
No.

Plant

Family

1.

Aloe vera

Asphodelaceae

2.

Acalypha indica Euphorbiaceae

Flavonoid present

Reference

Luteolin

20

Kaempferol glycosides: mauritianin, clitorin, nicrotiflorin, biorobin in its leaves and flowers

21

Quercetin, kaempferol; Quercetin-3-O- -D-glucoside, myricetin-3-O-rutinoside, quercetin-3-O-rutinoside,


kaempferol-3-O-rutinoside, kaempferol-3-O--D-glucoside and quercetin-3-O--L-rhamnoside in leaf;
isorhamnetin, myricetin, nimbochalcone
5-methoxy-7,8,2,3-tetramethoxyflavone, monohydroxytrimethylflavones, dihydroxy-di-methoxyflavone,
skullcaflavone; 5-hydroxy-7,8-dimethoxyflavanone and 5-hydroxy-3,7,8,2-tetramethoxyflavone, as well as
the known flavonoid 5-hydroxy-7,8- dimethoxyflavone.

3.

Azadirachta
indica

Meliaceae,
Zingiberaceae

4.

Andrographis
paniculata

Acanthaceae

5.

Bacopa
moneirra

Scrophulariaceae

Luteolin, luteolin-7-O- -glucopyranoside

21

6.

Betula pendula

Betulaceae

Quercetrin, myricetin galactoside, kaempferol, myricetin

26

7.

Butea
monospermea
Bauhinia
monandra

Fabaceae

Genistein, prunetine in stem bark

27

Fabaceae

Quercetin-3-O-rutinoside, Quercetin

28

9.

Brysonima
crassa

Malphigaceae

quercetin-3-O- -d-galactopyranoside, quercetin-3-O--l-arabinopyranoside, the biflavonoid amentoflavone,


(+)-catechin and ()-epicatechin, amentoflavone,
in leaves

29

10.

Calendula
officinalis
Cannabis
sativa

Compositae

Quercetin, isorhamnetin

26

Cannabaceae

Orientin, luteolin, luteolin-7-O- -glucopyranoside

21

12.

Citrus medica

Rutaceae

Seed consists of eriocitrin, hesperidin. Peel consists of neoeriocitrin, naringin, neohesperidin

13.

Clerodendrum
phlomidis
Clitoria
ternatea
Glyccheriza
glabra

Verbenaceae

Pectolinarigenin, 7-hydroxyflavone, 7-hydroxyflavonone, 7-O-glucoside

30

Fabaceae

Kaempferol-3-O- -glucoside, Quercetin-3-O- -glucoside, myricetin-3-O- -glucoside, isorhamnetin-3-O- glucoside, 3,5,7,4-tetrahydroxy-flavone-3-rhamoglycoside, kaempferol-3-neohesperidoside

Leguminosae

Liquiritin, isoliquiritin,liquritigenin,isoliquiritigenin, rhamnoliquiritin, liqcoumarin, 2-methylisoflavones

16.

Mimosa pudica

Mimosoideae

18.

Limnophila
indica

Scrophulariaceae

19.

Mentha
longifolia
Momordica
charantia
Oroxylum
indicum
Passiflora
incarnate

Lamiaceae

8.

11.

14.
15.

20.
21.
22.

Isoquercetin, avicularin, apigenin-7-O- -D-glucoside, cassiaocidentalin B, orientin, isoorientin in aerial


parts
(2S)-5,7,3,4-tetramethoxyflavone, 5,7,2,5-tetramethoxyflavone, 7-O-methylwogonin, skullcapflavone, 5hydroxy-7,20-dimethoxyflavone present in whole plant.
3,4-methlenedioxyflavone in roots and aerial parts
Luteolin-7-O-glycoside,luteolin-7,3-O-diglycoside, apigenin, quercetin-3-O-glycoside, kaempferol-3-Oglycoside; 5,7,4-trihydroxy-6,2,3-trimethoxyflavone

22,23
24, 25

25, 31
26
30
30
32, 33

Curcurbitaceae

Luteolin, kaempferol, quercetin (Agarwal),

34

Bignoniaceaea

Chrysin, baicalein, baicalein-7-O-glucoside, Oroxylin B

30

Passifloraceae

Vitexin, isovitexin, orientin, iso-orientin, 2- -D-glucoside

26

23.

Pongamia
pinnata

Fabaceae

Pongaflavonol , tunicatacatachalcone; Pongamone A-E, 5-hydroxy-40-methoxy-7-[(3-methyl-2-buthenyl)


oxy]-isoflavone, ovalichromene-B, pongachin, ponganone III, 5hydroxyfurano[7,6:4,5]flavone ,
pongaglabol, karanjin, pongapin, lancheolatin
B, 50-methoxypongapin, karanjachromene, pongachromene; luteolin;
(2S)-3,4-dimethoxy-6,6-dimethylpyrano[2,3:7,8]-flavanone , (2S)-6,3,4-trimethoxy-6,6dimethylpyrano[2,3:7,8]-flavanone, (2S)-7-methoxy-6-O-,-dimethylallyl-3,4-methylenedioxyflavanone,
2-hydroxy-3,4,5-trimethoxy-6,6-dimethylpyrano[2,3:4,3]chalcone, 2,4-dimethoxy-3,4methylenedioxydioxydihydrochalcone, 2,5,-trimethoxy-3,4-methylenedioxy-6,6dimethylpyrano[2,3:4,3]dihydrochalcone, 2,-dimethoxy-3,4-methylenedioxy-furano[2,3:4,3]dihydrochalcone, -hydroxy-2,4,6-trimethoxy-3,4-methylenedioxychalcone and 3-methoxy-furano[2,3:7,6]flavones present in roots

24.

Tephrosia
purpurea

Fabaceae

Purpurin, pongamol, isolonchocarpin,karanjin, lanceolatin-B, kanjone present in seeds

30

25.

Tilia cordata

Tiliaceae

Quercetrin, rutin, hyperoside, tiliroside, astragalin

26

27

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

PHARMACOLOGY OF FLAVONOIDS:
Reported

Pharmacological

activities

of

e-

O2

.O
2

H+

HO2.

flavonoids:

HO2. O2

Flavonoids have been reported to exert wide range of


biological

activities.

These

includes:

15],

11,

cytotoxic

neurodegenerative
[4,11,13,39].

antitumour,
diseases,

treatment

vasodilatory

[10,

of

action

In addition flavonoids are known to inhibit

lipid-peroxidation,

platelet

permeability

fragility,

and

aggregation,

Fig (V): Formation of peroxy radical

anti-

inflammatory, antibacterial, antiviral, antiallergic

capillary

cyclo-oxygenase

and

lipoxygenase enzyme activities. They exert these

Naturally, the organism has developed a defence


against toxic substances such as peroxynitrite and
nitrous acid. An important mechanism is catalyzed by
the enzyme superoxide dismutase (SOD), which
converts two superoxide anions to H2O2 and O2 [16] as
shown in fig (VI).

effects as antioxidants, free radical scavengers,


chelators of divalent cation

[15, 39, 40].

.O 2

hyalouronidase, alkaline phosphatise, arylsulphatase,


phosphodiesterase,

lipase,

Table 3: Reactive oxygen species that can be


scavenged or their formation can be inhibited by
flavonoids[43]

-glucosidase,

kinase [41].
1.

S.
No.

Flavonoids as antioxidants:

Mechanism of flavonoids as antioxidants:

[42].

This activity is attributed to their hydrogen-

donating ability. Indeed, the phenolic groups of

Reactive
species

Mechanism

1.

O2 (Superoxide
anion)

2.

HO2

3.

H2O2
(Hydrogen
peroxide)

4.

OH (Hydroxy
radical)

Flavonoids are powerful antioxidants against free


radicals and are described as free-radical scavengers

+ .O2-

flavonoids serve as a source of a readily available H


atoms such that the subsequent radicals produced can
be delocalized over the flavonoid structure [1].
Free

radical

scavenging

capacity

is

primarily
.

attributed to high reactivities of hydroxyl substituents


that participate in the reaction [8] as shown in fig (IV):
F-OH + R.

F-O. + RH

2H+

H2O2 + O2
SOD
Fig (VI): Mechanism catalysed by SOD

These are also

reported to inhibit variety of enzymes like hydrolases,


cAMP

H2O2.

5.
6.

(Alkoxy
RO
.
radical), ROO
(Peroxyl
radical)
1
O2

One-electron reduction product of O2.


Produced by phagocytes, formed in
autoxidation reaction and generated
by oxidases (heme proteins)
Protonated form of O2
Two electron reduction product of O2
formed from O2 by - dismutation or
directly from O2. Reactivity of O2 and
H2O2 is amplified in presence of heme
proteins
Three electrons reduction products of
O2 generated by Fentons reaction,
transition
metal
(iron,
copper)catalysed Haber-Weiss reaction; also
formed
by
decomposition
of
peroxynitrite produced by reaction of
O2 with nitric oxide radical.
.

Lipid peroxy radical (LOO ) produced


from organic hydroperoxide, ROOH by
hydrogen abstraction.
Singlet Oxygen

Fig (IV): Scavenging capacity of free radical (R.)


According to kinetic studies of aroxyl radical
Flavonoids inhibit lipid peroxidation in vitro at an

formation

and

decomposition

reactions,

the

early stage by acting as scavengers of superoxide

antioxidant capacity of a flavonoid is linked to its

anion and hydroxyl radicals. They terminate chain

three structural groups as shown in fig (VII).

radical reaction by donating hydrogen atom to a

1. The ortho-dihydroxy (catechol) structure in the B-

peroxy radical as in fig (V), thus, forming flavonoids

ring, which confers greater stability

radical, which, further reacts with free radicals thus

radicals, possibly through hydrogen bonding, and

terminating propagating chain [15, 6].

which participates in electron dislocation.

to aroxyl

2. The 2,3-double bond, in conjugation with a 4-oxo


function, responsible for electron dislocation from the
B-ring.
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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

3. The presence of both 3-(a)-and 5-(b)-hydroxyl

Ulcer is a commonly occurring disease in developed

groups (Fig.VII(c)).

countries and its occurrence is emerging with increase

(a)

OH

(b)

OH

OH

OH

b
OH

OH

OH

Etiology of gastric ulcer: The stress hormones like

epinephrine, norepinephrine, and ACTH, causes a

Fig VII: Structural groups responsible for


antioxidant activity [1]

vasoconstriction in the integument and the periphery,

3,4-catechol structure in B-ring strongly enhances


lipid peroxide inhibition and this arrangement is an
important characteristic of most potent scavengers of
peroxyl, superoxide and peroxynitrite radicals

[8]

and

its absence decreases antioxidant activity. The


absence of the hydroxyl group at position 3 in
flavanones and flavones decreases their antioxidant
ability[1].
Ghasemzadeh et al., reported that high level of total
phenolic

in modernisation of living standards.

HO

HO

OH

OH

OH

HO

OH

(c)

and flavonoid in Halia Bara variety

possessses potent antioxidant activities [44].


Bitis et al., isolated diosmetin, kaempherol, quercetin,
kaempherol 3-glucoside (astragalin), quercetin 3rhamnoside (quercitrin), quercetin 3-xyloside and
quercetin 3-galactoside (hyperoside) from Rosa
agrestis leaves and reported it to possess antioxidant
activity [45].
Shariffer et al., reported antioxidant activity of
methanolic extract of Teucrium polium and rutin and
apigenin were found to be potent inhibitors of lipid
peroxidation and oxidation of beta-carotene [46].
Braca et al., isolated several flavonoids from the leaves
of Licania licaniaeflora and reported quercetin
derivatives to possess strongest antioxidant activity
and flavonone 8-hydroxy-naringen and kaempferol 3O--rhamnoside possesses lowest antioxidant activity

whereas, they dilate the vessels of muscles, heart, and


brain. But, if the duration of this state gets prolonged,
then blood supply to major organs, e.g., stomach,
intestine, liver, kidneys, and skin get reduced and thus
failing to satisfy demand for oxygen, antibodies and
other agents that are required to maintain a healthy
condition.
As a result, the stress hormones increases the
glandular secretion which denatures proteins in
plasma membranes and catalyses the hydrolysis of
polysaccharide moieties of proteoglycans in the
protective mucous coat covering the luminal surface
of the stomach and the upper intestine to a perilous
extent during prolonged stress. When the walls of the
blood vessels supplying oxygen, nutrients, and
protective substances to this area gets sufficiently
weakened, then slight mechanical insults easily cause
ruptures, resulting in leakage of blood into the tissue.
Such events start inflammation and repair processes
in which eicosanoids, e.g., PGs, participate [16].
Flavonoids in treatment of gastric ulcer:
Flavonoids

inhibit

possess

strong

antioxidant

protein

influence protein phosphatase which reverses the


action of protein P-kinase as shown in fig (VIII):

FLAVONOID

epicatechin, epigallocatechin, galate, gallic acid,


quercetin-3-glucoside

of

phosphorylation. Inhibition of P-kinase signalling

[47].

Salucci et al., reported that dietary flavonoids like

regulation

(-) cAMP
(-) protein kinase C
(-) protein
phosphorylation
(-) COX

Inhibit gastric ulcer

Fig (VIII): Effect of flavonoids on gastric ulcer

activity [48].
Gulati et al., reported that quercetin at a dose of 15
mg/ 100g p.o. produced significant hepatoprotection
[49].

Flavonoids are favourable, effective, and usually


innocuous substitutes for the classical therapeutic
agents. It has also been reported that flavonoids

2. Effect of flavonoids on gastric ulcer:

29

protect against gastric cancer. Similar to aspirin,


acylated flavonoids may transfer their acyl group to

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

the side chain hydroxyl group of serine in the active


site of COX

battle against invasion by microorganisms or their

[16].

toxins which are recognised by specific antibodies

Flavonoids glycosides of Ocimum basilicum decreased

mounted on the surface of the macrophages in a

ulcer index and thus inhibit gastric acids in aspirin-

receptor

induced ulcers. Quercetin, Kaempferol, rutin when

associated with a second messenger producing

administered

enzymes

intraperitoneally

(25-100

mg/kg)

(FcR).
i.e.

Fc

receptor

is

non-covalently

phosphatidylinositol

lipase

which

inhibited dose-dependent gastric damage produced by

liberates inositol phosphates and diacylglycerol (DAG)

ethanol in rats [43].

from

the

plasma

membrane.

Several

inositol

phosphates activate specific protein phosphokinases


3. Effect of flavonoids on inflammation:

and DAG stimulates PKC.

Etiology: Inflammation is the integrated response of

complexes are endocytised, and raise the alarm in the

many defence systems of the body to the invasion of a

cell, with the result that the latter emits IL-1. This

foreign body. Inflammation involves action of the

substance induces the expression of the COX gene,

complement system, blood coagulation, humoral and

which encodes the PG COX that produces the

cellular

hormones,

eicosanoids, i.e., signal substances for the pain

angiogenesis, and repair processes. It is both a free

pathway (fig IX), chemotaxis, and smooth muscle

radical generating and free-radical producing process

contraction [16].

immunity,

cytokines,

tissue

The toxin-antibody

[50].

An important mechanism in inflammation is the


recruitment of macrophages to participate in the
MEMBRANE PHOSPHOLIPIDS
ARACHIDONIC ACID PATHWAY
FLAVONOIDS
CYCLOOXYGENASE
COX-1

LIPOOXYGENASE

COX-2

5-LOX
5-HPETE

PGG2

PGD2

PGE2

12-HETE

LTA4

PGH2

PGI2

12-LOX

PGF2

TXA2

LTE4

LTB4

Fig IX: Arachidonic acid pathway [51]


Flavonoids in treatment of inflammation:

catechins) have also been shown to have anti-

Flavonoids have been found to be prominent

inflammatory activity by inhibiting cycloxygenase-2

inhibitors of COX or LOX

[42, 45].

Flavonoids prevent

(COX2) and inducible nitric oxide synthase [52], which


[50].

synthesis of PGs that suppress T-cells. The immune

is related to antioxidant activity

cells communicate with chemical signals called

inhibit cytosolic and tyrosine kinase

cytokines

which

are

controlled

by

flavonoids.

inhibit neutrophil degranulation

[40].

Flavonoids also
[40, 53]

and also

The figure (X)

Flavonoids inhibit the activity of PKC at ATP-binding

represents the effect of flavonoids in the treatment of

site.

inflammation.

Flavonoids

[16].Various

also

promote

IFN

synthesis

flavonoids (e.g., quercetin, apigenin, tea

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

FLAVONOID

(-) COX
(-) iNOS
(-) cytosolic kinase
(-) tyrosine kinase
(-) neutrophil
degranulation
(-) protein kinase C
(+) Promote IFN
synthesis

head of the bone. These spikes cause tissue lesions,


bleeding, inflammation, and pain [16].
INHIBIT
INFLAMMATION

Flavonoids

in

treatment

of

Rheumatic

diseases: The beneficial effect of orally consumed


flavonoids includes the elimination of the PGs which

Fig X: Effect of flavonoids on Inflammation

mediate the pain. An additional effect of the


flavonoids

may

be

to

activate

cytotoxic

T-

Citrus flavonoids, hesperidin is known to possess anti-

lymphocytes, which kill cells presenting the harmful

inflammatory

Apigenin,

foreign antigen. Flavonoids do activate cytotoxic T-

luteolin, quercetin are known to possess anti-

lymphocytes, but the antigen, against which the

inflammatory activity [43].

lymphocytes are directed, remains unidentified

Guardia et al., reported quercetin and hesperedin

shown in fig (XI).

and

analgesic

effects.

[16]

as

given at a daily dose of 80 mg/kg inhibit both acute


and chronic phase of inflammation while rutin was

FLAVONOIDS

Activate Cytotoxic T-lymphocytes

found to be effective only in chronic case [54].


Kaempferol, quercetin, myricetin, fisetin are reported
to possess COX and LOX inhibitory activities [43].

Inhibit PGs

Kill T-cells prone to antigen

Fig (XI): Effect of flavonoids in Rheumatoid arithritis

4. Effect of flavonoids on rheumatic disease:

Kang

Etiology of Rheumatic disease: Autoimmunity

autoantigen-presenting and stimulatory functions of

and inflammation is an important component of

APCs necessary for activation and expansion of

rheumatoid arithritis. Since rheumatic disease is

autoreactive Th1 and Th17 cells and B cells and

associated with painful joints, it is believed that the

reported that it could suppress inflammation in

antigen specificity of the T-cells is directed against an

rheumatoid arithritis [53].Guardia et al., reported rutin

epitope characteristic of the cartilage in a joint, e.g., a

to be most effective plant flavonoids for the treatment

part of chondroitin sulphate.

of inflammation in chronic phase [54].

et

al.,

reported

that

apigenin

inhibits

IL-1 is produced by macrophages. It acts as a growth


hormone on T-lymphocytes, which are induced to

5. Flavonoids in treatment of thrombosis:

proliferate and secrete IL-2, which, in turn, is a

Etiology of Thrombosis: Arachidonic acid released

mitogen to T and B-lymphocytes, macrophages,

by in inflammatory conditions is metabolized by

granulocytes, and blood vessel endothelial cells.

platelets to form prostaglandin, endoperperoxides

Osteoclasts resembles macrophages because both

and thromboxane A2 thus contributing to platelet

produce and secrete IL-1 and are phagocytic. If

activation and aggregation. Platelet aggregation

osteoclasts respond to IL-2 secreted from immune

further contributes to atherosclerosis and acute

cells, then, the enhanced osteoclastic activity leads to

platelet thrombus formation. Activated platelets

the destruction of the heads of the long bones in the

adhering to vascular endothelium generate lipid

joints.

peroxides and oxygen free radicals which inhibit

In rheumatic arithritis, such a destruction is followed

endothelial function of prostacyclin and nitric oxide

by repair processes, which are uncoordinated with the

[40].

mechanical requirements defined by the stress


gradients. The topological activation pattern of the

Flavonoids

osteocytes leads to the formation of bony spikes in the

Flavonoids are used as antithrombotic due to their

in

treatment

of

thrombosis:

ability to scavenge free radicals. They inhibit


31

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

cyclooxygenase and lipooxygenase pathway. The main

Cancer

antiaggregatory

of

uncontrolled proliferation, dedifferentiation and loss

thromboxane A2 formation. Flavonoids like quercetin,

of function, invasiveness and metastasis that differ it

kaempferol and myricetin are known to possess

from normal cells [51].

effect

is

antiaggregatory properties

by

the

43].

[40,

inhibition

cells

manifest

to

varying

degree

of

The fig XII

represents mechanism of flavonoid in thrombosis.

Flavonoids in treatment of Cancer: Flavonoids


for a long time have been part of the herbal treatment

FLAVONOIDS

by lay practitioners, but they were recognised only


recently as effector substances. Examples of herbal
preparations owing their growing recognition as

(+) cAMP in platelets


(-) intracellular Ca++
(-) IP3 formation
(-)TxB2 formation
(-)TxA2 formation
(-) Phospholipase C
(-)PIP2 levels
(-) Intracellular
production of H2O2

effective anticancer drugs to flavonoids are propolis


(-) THROMBOSIS and
PLATELET
AGGREGATION

and Essiac [16].


Flavonoids are potent bioactive molecules that
possess anticarcinogenic effects since they can
interfere

with

the

initiation,

development

and

progression of cancer by the modulation of cellular


proliferation, differentiation, apoptosis, angiogenesis

Fig (XII): Effect of flavonoids on thrombosis

and metastasis [55] as shown in fig (XIII).


6. Effect of flavonoids on cancer-related
pathways:

Flavonoids

Etiology of Cancer: Cancer is a growth of diseases

to their ability to induce apoptosis[55].

caused by disturbance in growth metabolism

Normal cell

emerged

as

potential

chemopreventive candidates for cancer treatment due

[52].

Initiated cell

ROS scavenging , Alter carcinogen metabolism

have

Preneoplasts

Prevent further DNA damage


Induces apoptosis

Prevent further DNA damage,


Induces apoptosis
cell cycle arrest
Inhibit angiogenesis

Metastasis

Tumour
Prevent further DNA damage, Inhibit angiogenesis, Inhibit invasion

Fig XIII: Multistage of carcinogenesis and potential effects of polyphenols on cancer progression [55]
Flavonoids have been shown to be highly effective
scavengers of most types of oxidizing molecules,

OH

OH

OH
OH
HO

HO

O
HO

O
OH

including singlet oxygen and various free radicals,

OH
OH
OH

OH

O
OH

which are possibly involved in DNA damage and


tumor promotion. Flavonoids may also have a

Fig(XIV): Kaempferol Fig(XV): Quercetin Fig(XVI): Apigenin


OH

beneficial

effect

through

their

impact

on

the

bioactivation of carcinogens.
OH

The flavonols quercetin (fig XV), kaempferol (fig XIV)

Fig (XVII): Naringin

and galangin, and the flavones apigenin (fig XVI) have

Quercetin (fig XIV) and naringin (fig XVII) have also

been reported to inhibit cytochrome P450 enzymes of

been shown to inhibit CYP3A4, which is the most

the CYP1A family.

abundant P450 enzyme in the liver and beneficial in


metabolizing a significant number of carcinogens and
medications

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[16].

Quercetin is abundantly found in


32

Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

human diet and it gets extensively metabolized during

has been speculated that this classical hydrogen-

absorption in the small intestine and in the liver, and

donating antioxidant activity cannot account for the

thus exerts a dose-dependent inhibitory effect on cell

bioactivity of flavonoids in the brain as they are

[55].

In addition, animal and in vitro

present in very low concentrations. Instead, it has

studies have shown that tea catechins increase the

been postulated that their effects in the brain is

activity

mediated by an ability to protect vulnerable neurons,

proliferation
of

several

detoxifying

and

antioxidant

enzymes, such as glutathione reductase, glutathione

enhance

peroxidase, glutathione S-reductase, catalase, and

neuronal regeneration and induce neurogenesis.

quinone reductase

[16,

55].

In estrogen-dependent

existing

neuronal

function,

stimulate

Indeed, it has become evident that flavonoids are able

tumor cells or animal models, this anti-proliferative

to

effect has been related to the antiestrogenic properties

concentration via their interactions with critical

of certain flavonoids (e.g., isoflavonoids, quercetin).

neuronal intracellular signalling pathways pivotal in

In other in vitro models, flavonoids have also been to

controlling neuronal survival and differentiation,

affect cell-signaling and cell cycle progression. For

long-term potentiation and memory. Early indications

example, tea flavonoids inhibit signal transduction

regarding the ability of flavonoids to impact upon

pathways mediated by epidermal growth factor and

brain function were reported in the 1950s, with

platelet-derived growth factor, favorably affecting

flavones

exert

neuroprotective

reported
[14].

to

actions

act

as

even

novel

at

low

brain-stem

Studies suggest that flavonoids, in

downstream events such as angiogenesis. Genistein

stimulants

(fig XVIII) and quercetin inhibit protein tyrosine

particular isoflavones such as genistein might be

kinase which is also involved in cell proliferation [16, 55,

detrimental to memory processes in the brain due to

56].

Finally, apigenin, luteolin (fig XIX) and quercetin

their ability to act as tyrosine kinase inhibitors.

have been shown to cause cell cycle arrest and

Researches revealed that isoflavones results in

apoptosis by a p53-dependent mechanism [52].

positive effects on neuro-cognitive functions which is


apparent in post-menoupausal women. Activation of

OH
OH

HO

OH
HO

OH

both synaptic plasticity and new neural growth may


act together to enhance memory and cognition as

shown in fig (XX) [57].

O
OH

Fig (XVIII): Genistein

It has been found that flavonoids subclasses flavonols,

Fig (XIX): Luteolin

flavanols, flavanones, flavones and anthocyanins do


not exert exert oestrogen like effects and thus cannot

In a nutshell, multiple mechanisms have been

influence

identified for the anti-neoplastic effects of flavonoids,

mechanism.

including antioxidant, anti-inflammatory and antiproliferative activities, inhibition of bioactivating

memory

and

cognition

via

similar

SENSORY INFORMATION (EXPERIENCE)


AFFERENT NERVE INPUT

enzymes, and induction of detoxifying enzymes [52].


Increased Blood flow

Ghasemzadeh et al., studies have shown that some


flavonoids

components

such

as

quercetin

had

FLAVONOIDS

anticancer activities and were able to inhibit cancer

Angiogenesis
Neurogenesis

cell growth [46].


7. Effect of flavonoids on memory:
Flavonoids in treatment of memory cognition:
Historically, the biological actions of flavonoids to
their ability to exert antioxidant actions. However, it
33

Old neurons

Neuronal Maturation

Synaptic Activit

Functional integration

Synaptic plasticity

Immature neurons

New Synapses
Memory

Fig XX: Overview of functions of flavonoids on memory


system[57]

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

Jung et al., showed that quercetin at a dose of 10, 20,


40

mg/kg

p.o.

impairs

cognitive

function

(-) cAMP
(-)PDEase
(-) Ca++ dependent ATPase

FLAVONOID

by

suppressing pAkt and pCaMKII thus decreasing

PREVENT
ALLERGY

Fig (XXI): Effect of flavonoids on allergy

pCREB expression in hippocampus [49].


Maher et al., reported fisetin to facilitate memory by

The fig (XXI) depicts the mechanism of flavonoids in

activating ERK and inducing cAMP response element-

allergy. Quercetin prevents immune cells

binding protein phosphorylation [58].

inhibits both the production and release of histamine

[59]

and

and is useful in allergic conditions like asthma,


hayfever etc [60].

8. Effect of flavonoids on allergy:


Flavonoids in treatment of allergy: Flavonoids
inhibit cyclic AMP phosphodiesterase and calcium-

9. Effect of flavonoids on depression:

dependent

Etiology of Depression: Depression is caused by

ATPase

which

are

responsible

for

histamine release from mast cells and basophils [11].

functional deficiency of monoamine transmitters at


certain sites in brain [51] as shown in fig (XXII).

STRESS

CRF
release

GLUTAMATE

Hypothalamus

NMDA
receptor

ACTH
hormone

NA

5- HT

BDNF

2 receptor

5HT1A

TrkB
receptors

Signal Transduction Pathways


_

Pituitary
Detrimental gene
Cortisol
release

Beneficial gene

transcription response
+

transcription response
_

Neural apoptosis

+
Neurogenesis

DEPRESSIVE SYMPTOMS
Fig XXII: Pathophysiology of depression [51]

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

Flavonoids in treatment of depression:

propolis. It has been reported to possess inhibitory

Flavonoids have found to be ligands for GABAA

actions against Aspergillus tamarii, Aspergillus flavus,

receptors in the central nervous system and it led to

Cladosporium

hypothesis that they act as benzodiazepine-like

digitatum, Penicillium italicum [10].

sphaerospermum,

Pencillium

molecules. Many flavone derivatives were found to be


ligands for the GABAA receptors in the CNS; and thus

5,7,4-trihydroxy-8-methyl-6-(3-methyl-[2-butenyl])-

they bind to the benzodiazepine binding site with

2S-flavonone

resulting depressant actions in mice

[7].

These were

texana

isolated

and

from

shrub

flavonoids

Eysenhardtia

7-hydroxy-3,4-

also found to possess sedative action, tranquilizers,

(methylenedioxy) flavan isolated from Termanalia

anticonvulsant.

the

bellerica possess antifungal activity against Candida

spontaneous locomotor activity and thiopental-induce

albicans. 6,7,4-trihydroxy-3,5-dimethoxyflavone and

sleeping time effects obtained with the flavonoid

5,5-dihydroxy-8,2,4-trimethoxyflavone are effective

glycosides, the following decreasing order of action

against Aspergillus flavus [10].

Considering

the

sedative,

results:
2S-hesperidin>linarin>rutin>diosmin\cong2S-

Nobiletin and langeritin isolated from peelings of

neohesperidin> gossypin2S-naringin.

tangerine orange showed fungistatic action towards


Deuterophoma

Position of the sugar on the flavonoids nucleus seems


relevant as well and position-7 is the most effective
but the presence of a double bond between carbons 2
and 3, resulting in flavone derivatives with planar
configuration (i.e. linarin) does not appear to be
critical for activity. Flavonoid glycosides form the
newest group within the growing family of flavonoids
with activity on the CNS [7].

tracheiphila

stimulate fungal growth slightly

multiple neuroprotective actions in Central nervous


pathophysiological conditions including depression
and it was reported that naringenin possess potent
antidepressant-like property via central seotonergic
and noradrenergic system. It was further suggested
that dietary flavonoids possess a therapeutic potential
in disorders especially where monoaminergic system
is involve [61].

hesperidin

Quercetin, naringenin are reported to be inhibitors of


Bacillus subtilis, Candida albicans, Escherichia coli,
Staphylococcus nervous, Staphylococcus epidermis,
Saccharomyces cerevisiae [62].
Rattanachaikunsopon et al., isolated morin-3-Olyxoside,

morin-3-O-arabinoside,

quercetin-3-O-arabinoside

Yi et al., reviewed that dietary flavonoids possess

while
[43].

leaves

and

reported

from

that

quercetin,

Psidium

these

four

guajava
possess

bacteriostatic action action against all foodborne


pathogenic

bacteria

stearothermophilus,

including

Bacillus

Brochothrix

thermosphacta,

Listeria

monocytogenes,

Escherichia

coli,

Pseudomonas

fluorescens,

Salmonella

Staphyloccus aureus, Vibrio cholera

enteric,

[63].

Flavonones having sugar moiety showed antimicrobial


activity while none of the flavonols and flavonolignans

10. Effect of flavonoids on antimicrobial


activity:
Flavonoids have been used extensively since centuries

showed

inhibitory

activity

on

microorganisms.

Quercetin has been reported to completely inhibit


growth of Staphylococcus aureus [43].

for the treatment of various diseases. Propolis has


been used referred even in old testament for its
healing properties. The antimicrobial activity of
propolis has been attributed to its high flavonoids
content. Galangin is a flavonol commonly found in
35

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

Table 4: Antibacterial, antimicrobial and antiviral activities of flavonoids [41]


S. No.

Activity

Organism

Flavonoid

Staphylococcus aureus

1.

Antibacterial activity

2.

Antiviral activity

3.

Antifungal activity

Staphylococcus albus
Streptococcus pyogenes
Streptococcus viridians
Streptococcus jaccalis
Streptococcus baris
Streptococcus pneumonia
Pseudomonas aeruginosa
Escherichia coli
Baccilus subtilis
Bacillus anthracis
Proteus vulgaris
Clostrium perfingens
Rabies virus
Herpes virus
Para influenza virus
Herpes simplex virus
Respiratory synctial virus
Immuno-deficiency virus infection
Auzesky virus
Polio virus
Mengo virus
Pseudorabies virus
Candida albicans
Candida tropicalis
Fusarium solani
Botrytis cinerea
Verticillum dahlia
Azotabacter vinelandii
Alternacia tennisima
Cladosporium herbarum

Quercetin, Baicalin, Hesperitin, Fisetin, Naringin+rutin,


Naringin+hespertin, iso-liquiritigenin
Fisetin
Apigenin
Apigenin
Chrysin
Chrysin
Chrysin
Rutin,naringin,baicalin, hydroxyethylrutosine
Quercetin
Quercetin
Rutin
Datisetin
Hydroxyethylrutoside
Quercetin,quercetrin, rutin
Quercetin
Quercetin, rutin
Galangin, quercetin, kaempferol,apigenin
Quercetin,naringin
Apigenin
Quercetin, Quercetrin, morin, apigenin
Quercetin
Quercetin
Quercetin
Chloroflavonin
Quercetin
Chrysoeriol
Chrysoeriol
Chrysoeriol
Quercetin,rutin, epicatechin
Apigenin, Echinacin
Phaseolinisoflavan

11. Flavonoids in treatment of cardiovascular

transformation of xanthine dehydrogenase into ROS

diseases:

producing xanthine oxidase (XO) play important role

Cardiovascular diseases are today the principal cause

[16].

of death in both developing and developed countries.

Common consequences of AMI are heart failure and

CVS diseases include atherosclerosis, coronary heart

arrhythmias. Here again, ROS can mediate the cardiac

disease, arterial hypertension, and heart failure. The

hypertrophy and patients with heart failure have an

major reason behind CVS diseases is oxidative stress.

increased production of ROS. Similarly, ROS, and in

Oxidative stress is a condition of imbalance between

particular the superoxide radical, may play an

endogenous oxidants and reactive oxygen/nitrogen

important role in the genesis of some arrhythmias.

species (RONS) with predominance of reactive

Patients with arterial hypertension have an increased

species.

oxidative stress status [64].


Diseases:

Flavonoids in treatment of CVS: Studies ensure

Atherosclerosis involves modification of LDL particles

that long-term administration of flavonoids can

by oxidative stress with subsequent induction of

decrease, or tend to decrease the incidence of

inflammation which is caused by increased leucocyte

cardiovascular diseases and their consequences.

Etiology

of

Cardiovascular

adherence [16].
Endothelial

dysfunction

with

increased

platelet

aggregation facilitates procoagulation, which may


induce a thrombosis resulting in an acute myocardial
infarction. In the ischemic phase of AMI platelet
aggregation, the activation of neutrophils, an increase
in

cellular

free

redox

active

iron,

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and

the

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

Table 5: Proposed positive effects of flavonoids on CVS:


S. No.

Cardiovascular diseases

Influence of flavonoids

1.

Atherosclerosis

Decrease in LDL oxidation by LOX inhibition and attenuation of oxidative stress, inhibition of
leucocyte leucocyte adhesion, myeloperoxidase, decreased expression of iNOS and COX-2

2.

Acute myocardial infarction

Decrease in ROS burst, inhibition of platelet aggregation

3.

Heart Failure

Decrease in oxidative stress (direct ROS scavenging) inhibition of metalloproteinase

4.

Arrhythmia

Decrease in oxidative stress

5.

Hypertension

Vasodilatory properties, inhibition of NADPH oxidase, recovery of NO due to inhibition of superoxide


production

Flavonoid consumption prevent many cardiovascular

stimulate Ca2+ uptake from isolated islet cells thus

diseases including hypertension and atherosclerosis.

suggesting it to be effective even in non-insulin

Quercetin

dependent diabetes [43].

protects

LDL

against

oxidative

modifications effect. 7-monohydroxyethylrutoside and

Li et al., indicated that flavonoids in Ipmoea batalas

7, 3, 4-trihydroxyethylrutoside are reported to be

leaf possesses antidiabetic activity against alloxan-

cardioprotective

[43].

induced diabetes at a dose of 100 mg/kg [67].


Sriram et al., reported fisetin to be a therapeutic agent

12. Effect of flavonoids on diabetes mellitus:

for treatment of diabetes mellitus at a dose of 10

Etiology of diabetes mellitus: Diabetes mellitus is

mg/kg [68].

a serious chronic disease. Effective control of the


blood glucose level is a key step in preventing or

13. Effect of flavonoids in treatment of

reversing diabetic complications and improving the

hepatotoxicity:

quality of life in both types 1 and 2 diabetic patients

Role

[65].

hepatotoxicity: Flavonoids bind to subunit of DNA-

Flavonoids in treatment of diabetes mellitus:

dependent RNA polymerase I, thus activating the

All flavonoids cannot cure diabetes mellitus because

enzyme. As a result, protein synthesis gets increased

most types of this disease are basically genetic and no

leading to regeneration and production of hepatocytes

single drug can correct an inborn error. However,

[11].

flavonoids can ameliorate some of the consequences

Silymarin,

flavonoids

apigenin,

in

treatment

quercetin,

naringenin

of

are

Flavonoids have been

reported to be potent therapeutic agents against

identified to be good inhibitors of aldose reductase

microcrystin LR-induced hepatotoxicity. Rutin and

[66].

venoruton are reported to show regeneration and

of diabetes mellitus

[16].

of

The fig (XXIII) depicts the mechanism of

hepatoprotective effects in experimental cirrhosis [43].

flavonoids in diabetes mellitus.

FLAVONOID

(-) Aldose reductase,


Regenerate pancreatic
islets,
(+) insulin release,
(+) Ca++ uptake

Gulati et al., studied hepatoprotective studies on


PREVENT
DIABETES
MELLITUS

Phyllanthus emblica and quercetin and quercetin and


found that if the extract is producing hepatoprotection
at a dose of 100 mg/ 100 g p.o., then quercetin is
producing hepatoprotection at a dose of 15 mg/ 100 g

Fig (XXIII): Effect of flavonoids on diabetes mellitus

p.o.; thus concluding that quercetin is a potent

It has been reported by several researchers that

hepatoprotective agent [69].

quercetin possess antidiabetic activity and it has been

Kim et al., isolated isovitexin, hirustin, trifolin,

found that it brings about regeneration of pancreatic

avicularin and quercetin. It was observed that

islets and increases insulin release in streptozotocin-

hirustrin,

induced diabetes. Also, it has been reported to

hepatoprotective action

37

avicularin,

Internationale Pharmaceutica Sciencia

quercetin

possess

against t-BHP in HepG2

Jan-Mar 2011

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Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

cells, whereas isovitexin and trifolin possess no


protective effect

[70].

[10].

phytochemicals on an individual basis

Flavonoids

are found to be toxic to cancer or immortalized cells


[40].

Due to the low

Oh et al., 2004 reported that among various

but are less toxic to normal cells

flavonoids i.e. apigenin, luteolin, kaempherol-3-O-

solubility of flavonoid aglycones in water, to the short

glucoside and quercetin-3-O-glucoside isolated from

residence time of flavonoids in the intestine, and to

Equisetum arvense, onitin and luteolin exhibited

the low coefficient of absorption, it is not possible for

hepatoprotective

humans to suffer acute toxic effects from the

activity

against

tacrine-induced

cytotoxicity in human liver-derived Hep G2 cells [57].

consumption of flavonoids, with the exception of a


rare occurrence of allergy. The margin of safety for the

Toxicological Profile of flavonoids:

therapeutic use of flavonoids in humans, therefore, is

Flavonoids are widely distributed in edible plants and

very large and probably not surpassed by any other

beverages

drug in current use [16].

and

have

been

previously

used

in

traditional medicines, so they are believed to be nontoxic

[10, 15].

However, this family of compounds

CONCLUSION

possess a diverse range of activities in mammalian

Flavonoids constitute a wide array of biological active

cells. So, in-vivo confirmation of their side effects

compounds that are found abundantly in plant

would be necessary for full evaluation of their

kingdom and dietary intake. They are gaining interest

practical usefulness in the field of modern medicine.

due to their wide variants and number of members.

Given that the selectivity of flavonoids for eukaryotic

These are reported to be effective in pathogenesis of

enzymes

to

majority of disases. Antioxidant activity is the

compound, a study regarding assessment of its

foundation of many actions which lead to its

toxicity

beneficial effects in majority of the diseases.

appears
is

to

required

vary
to

from
be

compound

done

on

these

Table 6: Diseases treated with Flavonoids


S.
No.

Disease

1.

Ulcer

2.

Rheumatoid arithritis

3.

Inflammation

4.

Cancer

5.

Memory dysfunction

6.

Depression

7.

Cardiovascular
diseases

8.

Diabetes mellitus

9.

Antiallergic

10.

Hepatoprotective

11.
Thrombosis

Flavonoid
Kaempferol,
(+)-Cyandidanol-3, meciadanol, catechins
Sofalcone, Quercetin
Apigenin, rutin
Quercetin, apigenin, catechin
Hesperidin,rutin, luteolin
Kaempferol, quercetin, myricetin, fisetin
Quercetin, Kaempferol, Galangin, Apigenin
Quercetin, naringin
Genistein, Quercetin
Apigenin, luteolin, quercetin
Catechins
Genistein
Quercetin
Fisetin
Naringenin,
2S-hesperidin, Linarin
Quercetin
7-monohydroxyethylrutoside,
7,3,4-trihydroxyrutoside
Fisetin
Quercetin
Quercetin
Rutin, citrin
Disodium cromoglycate
Quercetin
Avicularin, hirustrin
Onitin, luteolin
Tangeratin, hesperidin, quercetin, rutin
Trihydroxyethylrutoside, O-( hydroxyethyl)rutoside, (+)-catechol
Nobelitin, sinesetin

Internationale Pharmaceutica Sciencia

Jan-Mar 2011

Target
PAF
Gastric H+/K+ ATPase
PG synthesis
Suppress inflammation by acting on COX
COX and iNOS
PG synthesis
+

Na /K ATPase, Cyt P450


Cyt P3A4
Tyrosine kinase
P53 dependent
Glutathione reductase, glutathione peroxidise,
catalase, quinine reductase
Tyrosine kinase
pAKt and pCREB
ERK and cAMP response element
------------------------LDL
Aldose reductase
Mast cell
Capillary wall
+
H ATPase
------------------------Horse erythrocytes
Blood vessels
Erythrocyte aggregation
Vascular permeability

Vol 1 Issue 1

Reference
41, 43
41
41, 43
54, 53
50, 52
43, 54
43
16
16
16,55, 51
46, 52
16, 55
49
49
58
61
7
43
68,
41
58, 59
41
41
69, 71
71
71
41

38

Bimlesh Kumar, et al: A Review of Phytochemistry and Pharmacology of Flavonoids

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