Indian Journal of Biochemistry & Biophysics

Vol. 47, April 2010, pp. 104-109

Hypolipidemic and antioxidant activity of Anthocephalus indicus
(Kadam) root extract
Vishnu Kumar
1
, Farzana Mahdi
1
, Ramesh Chander
1
, Ranjana Singh
2
, Abbas Ali Mahdi
2
, Ashok Kumar Khanna
3
,
Sanjay Bhatt
4
, Rajeev Singh Kushwaha
4
, Kalbe Jawad
5
, Jitendra Kumar Saxena
3
and Raj Kumar Singh
4*

1
Department of Biochemistry, Eras Lucknow Medical College & Hospital, Lucknow 226001
2
Department of Biochemistry, CSM Medical University, Lucknow 226003
3
Division of Biochemistry, Central Drug Research Institute, Lucknow 226003
4
Department of Biochemistry, Shri Guru Ram Rai Institute of Medical & Health Sciences, Patel Nagar, Dehradun 248001
5
Department of Biochemistry, UP Rural Institute of Medical Sciences & Research, Saifai, Etawah, UP 206301


Received 06 November 2009; revised 03 March 2010
The present study was carried out to explore the anti-diabetic, anti-dyslipoproteinemic and anti-oxidant activities of
Anthocephalus indicus root extract in alloxan-induced (150 mg/kg body wt.) diabetic rats. A marked increase in plasma
levels of glucose and lipid peroxides accompanied with an elevation in the lipids and apoprotein levels of serum very low
density lipoprotein (VLDL) and low density lipoprotein (LDL) following decrease in lipid and protein constituents of high
density lipoprotein (HDL) were observed. The alterations in lipoprotein pattern was associated with inhibition of lipolytic
and antioxidant enzymes. Oral administration of root extract (500 mg/kg body wt.) for 30 days in dyslipidemic animals
resulted in significant decrease in plasma glucose, total cholesterol, phospholipids, triglyceride and lipid peroxides. The
decrease of lipids and apoprotein levels of VLDL and LDL were followed by stimulation of plasma post-heparin lipolytic
activity and lecithin cholesterol acyltransferase as well as hepatic superoxide dismutase and catalase activities. Lipid and
apoprotein levels of HDL were also recovered partially on treatment with root extract.
Keywords: Cholic acid, Deoxycholic acid, Lipid peroxides, Superoxide dismutase, Catalase, Lipoprotein lipase,
Triglyceride lipase, Lecithin cholesterol acyltransferase.
Anthocephalus indicus (Family: Rubiaceae) is
commonly known as Kadam and its roots, bark,
leaves and fruits have been used in Ayurvedic remedy
for skin diseases and metabolic disorders and also
mentioned in many other ancient Indian medical texts
to possess antidiarrheal, detoxifier, analgesic and
aphrodisiac properties
1,2
. The plant is found
abundantly throughout India, especially at low
altitude and in humid places. In traditional system of
medicine, warm aqueous extract of leaves has been
used to alleviate the pain, swelling and for cleansing
and healing of wounds and in treatment of
menorrhegia. The decoction of bark is effective in
diarrhea, dysentery and colitis. The root extract is
helpful in urinary ailments like dysuria, calculi and
glycosuria.
The heartwood and leaves contain 3 and 3
isomers of dihydrocadambine
3,4
and stem bark
cadambagic acid, quinovic acid and sitosterol
5
.
A complex polysaccharide from flower and seeds has
also been isolated
6
. The above-mentioned compound
(cadambagic acid, quinovic acid, sitosterol, 3 and
3 isomers of dihydrocadambine) of the plant may be
responsible for its antidiarrheal, detoxifier, analgesic
and aphrodisiac properties. Furthermore, fruit juice
augments the quality of breast milk of lactating
mothers and act as a lactodepurant
7
. Recently, we
reported that alcoholic extract of A. indicus root exerts
hypoglycemic activity in alloxan-induced diabetic rats
and hypolipidemic activity as well as anti-oxidant
activity
8-10
.
Diabetes mellitus (DM) is a chronic disease caused
by the inherited and/or acquired deficiency in
production of insulin by pancreas or by the

*Corresponding author
E-mail: singhrk23a@hotmail.com
Tel: +91-135-2522168 (0) ; Fax: +91-135-2522117.
Abbreviations: CAT, catalase; DM, diabetes mellitus; FFA, free
fatty acid; HDL, high density lipoprotein; LCAT, lecithin
cholesterol acyltransferase; LDL, low density lipoprotein; LPL,
lipoprotein lipase; LPL, lipoprotein lipase activity; LPO, lipid
peroxides; PHLA, post-heparin lipolytic activity; PL,
phospholipids; SOD, superoxide dismutase; TC, total cholesterol;
TG, triglyceride; TGL, triglyceride lipase; VLDL, very low
density lipoprotein.
KUMAR et al.: HYPOLIPIDEMIC AND ANTI-OXIDATIVE EFFECT OF ANTHOCEPHALUS INDICUS ROOT


105
ineffectiveness of the insulin produced, which leads to
hyperglycemia and at later stages lipid metabolism is
also affected
11,12
. DM in human and experimental
models also increased oxidative stress due to
persistent and chronic hyperglycemia
13
, and protein
glycation
14
due to depletion of antioxidant defense
system
15
, thus promotes de novo free radical
generation
16
. Current therapies used for controlling
diabetic complications are associated with several
side effects
17
. Moreover, as synthetic antioxidants are
suspected to be carcinogenic
18
, there is a need for
effective, safe and better oral hypoglycemic agents.

Herbal formulations are preferred due to lesser side
effects and their low cost. One of the etiologic factors
implicated in the development of diabetes and its
complications is the damage induced by free radicals.
Thus, a drug having multi-fold properties such as anti-
diabetic, lipid lowering and antioxidant activities is in
great demand. Therefore, in the present study, an
attempt has been made to explore hypolipidemic and
antioxidant activities of Anthocephalus indicus
(Kadam) root extract.

Material and Methods
Alloxan monohydrate and standard drug
glibenclamide were procured from Sigma Chemical
Co., St. Louis, MO, USA.

Preparation of root extract
A. indicus (secondary and tertiary) roots were
collected from local area of Lucknow and identified
taxonomically by the Department of Pharmacology,
Eras Lucknow Medical College & Hospital,
Lucknow and a voucher specimen was also submitted
to Department of Pharmacology, Eras Lucknow
Medical College & Hospital, Lucknow (AI-001/06).
Roots were dried under shade and made into fine
powder using laboratory mill and powder (250 g) and
extracted thrice with 1500 ml portions of 95% ethyl
alcohol in a laboratory percolator at room
temperature
9
. Time allowed for each extraction was
8 h. The root extract obtained after third extraction
was colorless. All the extracts were mixed (total
amount of solvent of 3 extractions were 1500 ml),
alcohol was distilled out at reduced temperature
(20C) and reduced pressure (100 psi) in a rotor
evaporator. The whole mass was then taken out in a
pre-weighed beaker and subjected to vacuum drying
for 6 h which yielded 16 g of crude extract, which
was used for in vivo and in vitro studies.
Animals and treatment
Animal study was performed with the approval of
Animal Care Committee of Division of Laboratory
Animal, Central Drug Research Institute, Lucknow,
India and confirmed to the guidelines for Care and
Use of Laboratory Animals of the Institute. Male
adult rats of Charles Foster strain weighing
200-225 g bred in the animal house of the Institute
were used. The rats were divided into four groups
having six animals each as follows: Group 1:
Control rats; Group 2: Diabetic rats (on normal
saline); Group 3: Diabetic rats + A. indicus
(500 mg/kg b.w.)
8-10
; Group 4: Diabetic rats +
Glibenclamide (600 g/kg b.w.)
20
. After 30

days of
feeding rats were fasted overnight and blood was
withdrawn from the retro-orbital plexus. A group of
normal rats without treatment with alloxan were also
included to serve as control. These animals were
housed in polypropioline cages and kept in uniform
hygienic conditions, temperature 25-26C, relative
humidity 60-70% and 12/12 h light/dark cycle (light
from 08:00 to 20:00) and provided with standard
pellet diet (Lipton India Ltd.), and water ad libitum.
Diabetes was induced in rats by a single
intraperitonial injection of alloxan monohydrate
150 mg/kg b.w. in 18 animals. After 2 weeks, rats
with serum glucose level 280-367 mg/dl were taken
for the study
19
.

Biochemical analysis
Serum from above rats was fractionated into very
low density lipoprotein (VLDL), low density
lipoprotein (LDL) and high density lipoprotein (HDL)
by polyanionic precipitation method
21
. Serum as well
as lipoproteins were analyzed for their total
cholesterol (TC)
22
, triglyceride (TG)
23
, phospholipids
(PL)
24
and apoprotein
25
. Serum lipid peroxides
(LPO)
26
, free fatty acid (FFA)
27
, plasma protein
28
,
plasma lecithin cholesterol acyl transferase (LCAT)
activity
29
and PHLA
30
were also estimated.
Liver homogenized (10% w/v) in cold 1 M
phosphate buffer (pH 7.2) was used for the assay of
lipoprotein lipase (LPL)
30
and triglyceride lipase
(TGL)
31
activities. Liver homogenate 10% w/v in
0.15 M KCl was also used for the estimation of
superoxide dismutase (SOD)
32
and catalase (CAT)
33
.
The lipid extract of each homogenate was used for the
estimation of TC, PL and TG by above-mentioned
methods. The rats faeces spilling from all groups over
30 days were collected and processed for the
quantification of cholic and deoxycholic acid
34
.
INDIAN J. BIOCHEM. BIOPHYS., VOL. 47, APRIL 2010


106
Statistical analyses
One-way-analysis of variance (ANOVA-
Newmans student test) was performed by
comparison of values for alloxan-treated group with
control, alloxan and drug-treated with alloxan only.
All hypothesis testing were two-tailed. P<0.05 was
considered statistically significant and the results
were expressed as mean SD. The Graph pad
INSTAT 3.0 software was used to carried out the
statistical analysis
35
.

Results

Effect of root extract on serum lipid, FFA, LPO and plasma
protein in alloxan induced diabetic rats
Table 1 shows that acute administration of alloxan
markedly increased in the plasma TC, TG and PL
levels (79% 12.16, 98% 17.02 and 29% 12.04,
P<0.001), FFA (52% 4.09, P<0.001), LPO, (233%
46.78, P<0.001), and decreased plasma protein
(31% 4.89, P<0.001). However, treatment with
A. indicus root extract caused reversal in the levels of
TC (21% 3.17), PL (20% 8.70, P<0.05), TG (29%
9.80, P<0.001), FFA (9% 1.60), LPO (35%
12.35, P<0.001) and protein by 4% 1.00.
Glibenclamide reversed the levels: TC (18.0%
3.13), TG (24.0% 9.270, P<0.05), PL (4.0%
2.18), FFA (27% 3.62, P<0.001), LPO (38%
12.28, P<0.001) and protein (8.0% 1.45).

Effect of root extract on serum lipoprotein profile in alloxan-
induced diabetic rats
Analysis of hyperglycemic serum (Table 2) showed
marked increase in the levels of lipids and apoprotein
constituting -lipoproteins (VLDL and LDL) in
alloxan-treated group and these effects were more
pronounced for VLDL-TC, PL and TG (50% 14.25,
28 11.43 and 90% 13.30, P<0.001 respectively)
and apoprotein (17% 6.36, P<0.05). There was
increase in LDL-TC, PL, TG (300% 88.82, 45%
10.49, 90% 13.26, P<0.001 respectively) and
apoprotein (20% 4.80, P<0.05). The decrease in
Table 1Effect of A. indicus root extract on serum lipid, protein, lipid peroxides and FFA levels in alloxan-induced diabetic rats
[Values expressed as mean SD of 6 animals]
Experimental schedule Total cholesterol
(mg/dl)
Triglycerides
(mg/dl)
Phospholipids
(mg/dl)
Protein
(g/dl)
Serum lipid peroxides
(n mol MDA/ml
plasma)
Serum free
fatty acid
( mol/L)
Control 84.23 10.66 87.72 7.54 96.76 11.30 7.13 0.45 2.73 0.49 1.68 0.17
Alloxan-treated 148.15 26.80 ** 173.81 13.60 ** 124.88 14.68 ** 4.94 0.36 ** 8.98 1.40** 2.56 0.30**
Alloxan + A. indicus
(500 mg/kg b.w.)
117.13 20.29 * 123.46 9.60 ** 100.25 19.57* 5.48 0.39
NS
5.80 0.99** 2.32 0.38
NS

Alloxan + glibenclamide
(600 g/kg b.w.)
122.18 18.86* 131.78 11.24* 119.45 11.67
NS
5.67 0.69
NS
5.55 0.99** 1.88 0.29**
Alloxan-treated group was compared with control, alloxan and drug-treated group with alloxan. *P<0.05, **P<0.001,
NS

= Non-significant.
[
Table 2Effect of A. indicus root extract on lipoprotein profile in alloxan-induced diabetic rats
[Values expressed as mean SD of 6 animals]
Experimental
schedule
VLDL LDL HDL
TC
(mg/dl)
PL
(mg/dl)
TG
(mg/dl)
Apo-
protein
(mg/dl)
TC
(mg/dl)
PL
(mg/dl)
TG
(mg/dl)
Apo-
protein
(mg/dl)
TC
(mg/dl)
PL
(mg/dl)
TG
(mg/dl)
Apo
protein
(mg/dl)
Control 8.08
0.63
16.43
1.99
39.10
3.95
6.85
1.04
17.07
1.78
11.48
1.11
20.12
1.11
17.13
1.61
51.53
3.80
39.97
3.35
14.47
1.43
173.83
11.34
Alloxan-treated 12.09
***
1.20

20.92***
2.48
73.76***
5.70
8.00*
0.57
68.68***
8.65
16.59***
1.43
37.21***
6.29
20.55*
1.46
38.71***
3.75
30.52***
2.27
12.55*
1.28
127.42***
12.33
Alloxan + A.
indicus
9.19***
0.76
16.75
1.37 **
57.90
4.70 **
7.44
NS
0.76
39.25***
3.50
13.36**
1.06
30.17**
6.68
17.50
NS
2.07
43.42NS

4.25
33.84
NS
3.01
13.61
NS

1.29
151.25*
15.67)
Alloxan +
glibenclamide
10.04
0.96*
20.30
NS
2.39
52.02***
5.62
7.20
*

0.86
42.33
***
3.80

16.44
NS
1.40

28.24***
4.36
18.70
NS

1.52
41.00
NS

4.22
31.12
NS

1.55
13.50
NS
1.28

141.16
NS

12.41
Alloxan-treated group was compared with control, alloxan and drug-treated groups with alloxan. ***P<0.001, **P<0.01, *P<0.05,
NS= Non significant.
KUMAR et al.: HYPOLIPIDEMIC AND ANTI-OXIDATIVE EFFECT OF ANTHOCEPHALUS INDICUS ROOT


107
HDL-TC, PL, apoprotein (25% 3.86, 24% 6.84,
27% 3.69 respectively; P<0.001), and TG (13%
2.73, P<0.05) was also observed.
The results in Table 2 also show that treatment
with A. indicus roots extract for 30 days significantly
reversed the level VLDL-TC (24% 3.40, P<0.001),
PL, TG (20% 2.31, 21% 1.88, respectively;
P<0.01) and apoprotein (8% 2.76). There was also
decrease in LDL-TC (43% 9.94, P<0.001), PL, TG
(19% 4.51, 19% 7.53, P<0.01) and apoprotein
(15% 8.26). A. indicus roots extract increased the
levels of HDL-TC, PL, TG (12% 2.73, 11% 2.62,
8% 0.94 respectively), and apoprotein (16% 1.23,
P<0.05). Glibenclamide decreased VLDL-TC,
apoprotein (17% 1.32, 11% 7.30 respectively;
P<0.05), PL (3% 0.48) and TG (29% 1.16,
P< 0.001), LDL-TC, and TG (38% 5.76, 24%
3.00 respectively, P<0.001), PL and apoprotein
(0.9% 0.52, 9.0% 7.59, respectively) with
simultaneously increase in HDL-TC, PL, TG, and
apoprotein (6% 2.30, 2% 0.43, 7% 1.06, 10%
2.01, respectively) .

Effect of root extract on hepatic SOD, CAT, TGL and LPL in
alloxan-induced diabetic rats
The data in Table 3 show that administration of
alloxan in rats inhibited the activities of SOD (24%
7.71, P<0.001), CAT (25% 12.76, P<0.001), TGL
(20% 1.83, P<0.05) and LPL (25% 3.17,
P<0.001) respectively. The treatment with A. indicus
roots extract for 30 days increased SOD (25% 8.43,
P<0.01), CAT (19% 1.76, P<0.05), TGL (17%
2.09, P<0.05) and LPL (21% 3.16, P<0.001).
Glibenclamide decreased the activities of SOD
(26% 8.76, P<0.01), CAT (27% 9.02, P<0.01),
TGL (17% 4.33, P<0.05) and LPL (23% 3.16,
P<0.05, respectively).

Effect of root extract on faecal bile acids, plasma LCAT,
PHLA in alloxan induced diabetic rats
Administration of alloxan in rats markedly
decreased in the levels of cholic acid (30% 4.61,
P<0.01) and deoxycholic acid (38% 2.19) in feces,
as well as LCAT (33% 1.27, P<0.01) and PHLA
(28% 1.27, P<0.01) in plasma. The treatment with
A. indicus roots extract for 30 days increased the
levels of cholic acid (17% 3.93, P<0.01) and
deoxycholic acid (17% 2.17, P<0.01) in feces and
LCAT (14%1.64, P<0.01) and PHLA (13% 1.47,
P<0.01) in plasma of alloxan-induced diabetic rats.
Glibenclamide decreased the levels of cholic acid
(28% 1.22, P<0.01) and deoxycholic acid
(28%3.02) in feces also and LCAT (29% 8.29,
P<0.01) and PHLA (25% 7.47, P<0.01) in plasma
(Table 4).
Table 3Effect of A. indicus root extract on hepatic SOD, CAT, TGL and LPL in alloxan-induced diabetic rats
[Values expressed as mean SD of 6 animals]
Experimental schedule SOD
(Unit/min/mg protein)
CAT
(Unit/min /mg protein)
TGL (n mol FFA
released/h/mg protein)
LPL (n mol FFA
released/h/mg protein)
Control 2.80 0.20 3847 248.17 74.11 5.78 85.69 7.71
Alloxan-treated 2.14 0.16*** 2873 402.08*** 59.63 4.62* 66.36 5.46**
Alloxan + A. indicus 2.69 0.10** 3403 499.69* 69.74 5.18* 80.02 9.81**
Alloxan + glibenclamide 2.70 0.13** 2625 482.02** 69.85 7.08* 81.89 8.68*
Alloxan-treated group was compared with control, alloxan and drug treated group with alloxan.*P<0.05,* *P<0.01, ***P<0.001.
[
Table 4Effect of A. indicus root extract on faecal bile acids, plasma lecithin cholesterol acyltransferase and plasma post-heparin
lipolytic activities in alloxan-induced diabetic rats
[Values expressed as mean SD of 6 animals]
Experimental schedule Faecal bile acids Plasma lecithin cholesterol acyl
transferase activity
(n mol cholesterol released/h/l)
Plasma post-heparin
lipolytic activity
(n mol FFA formed/h/l)
Cholic acid
(g/g feces)
Deoxycholic acid
(g/g feces)

Control 76.31 6.86 56.76 11.36 61.57 4.92 15.19 1.19
Alloxan-treated 53.68 6.49** 35.34 7.83** 41.04 3.76** 10.96 0.98**
Alloxan + A. indicus root
extract (500 mg/kg b.w.)
62.70 1.90** 41.40 3.81** 46.75 4.92* 12.40 0.91*
Alloxan + glibenclamide
(600 g/kg b.w.)
68.69 3.81** 44.81 2.08** 53.00 1.23** 13.75 1.16**
Alloxan-treated group was compared with control, alloxan and drug-treated group with alloxan. *P<0.05, ** P<0.01.

INDIAN J. BIOCHEM. BIOPHYS., VOL. 47, APRIL 2010


108
Discussion
Alloxan selectively damages the -cells and
suppresses the production of insulin in pancreas, thus
is used to induce diabetes in laboratory animals. This
occurs most likely because of selective uptake of the
alloxan, due to its structural similarity to glucose as
well as highly efficient uptake mechanism in -cells.
However, alloxan is not toxic to human -cells, even
in very high doses, probably due to differing glucose
uptake mechanisms in human and rodents
36
.
In our experiment, we observed higher levels of
serum lipids in alloxan-treated diabetic rats. The level
of serum lipids is usually raised in diabetes and such
an elevation represents a risk factor for cardiovascular
diseases
37
. Lipases play a significant role in
lipoprotein metabolism and decreased lipoprotein
lipases activities in diabetes is main cause of
atherosclerosis
38
. In case of DM, PHLA, serum LPL,
HTGL, sciatic nerve LPL and adipose tissue LPL
activities have been found to decrease
39
. On the other
hand, pancreatic lipase and co-lipase activities
increase in pancreatic acinar tissues of diabetic rats
40
.
In the present study, activities of SOD and CAT were
found to decrease in alloxan-induced diabetic rats and
similar observations were reported by other workers
41
.
The treatment with A. indicus recovered the activity
of these antioxidant enzymes in alloxan-induced
diabetic rats.
The abnormal high concentration of serum lipid in
diabetes is mainly due to the increase in the
mobilization of free fatty acid from the peripheral
depots, since insulin inhibits the hormone sensitive
lipase
42
. On the other hand, glucagon, catecholamine
and other hormones enhance lipolysis. The marked
hyperlipidemia that characterizes the diabetic state
may, therefore, be regarded because of the
unregulated actions of lipolytic hormones on the fat
depots
42
. In the present study, we also observed higher
levels of blood glucose, TC, TG, PL and FFA in
alloxan-induced diabetic rats. Similar results also
have been reported by other workers in alloxan-
induced diabetic rats
19
.
A. indicus root and glibenclamide both caused a
significant decrease in the plasma levels of TC, TG,
PL and FFA in alloxan-induced hyperglycemia. In
alloxan-induced diabetic rats, A. indicus increased the
level of HDL by stimulating the activity of LCAT,
which might contribute to the regulation of blood
lipids. LCAT play a key role in lipoprotein
metabolism and most of the lipoprotein changes are
the outcome of primary abnormality owing to the
diseases related with lipid metabolism
43
. A. indicus
enhanced the excretion of bile acids through feces and
this contributed to regress the cholestesteosis in liver
damage.
In conclusion, the lipid lowering activity of
A. indicus might be due to inhibition of hepatic
cholesterol biosynthesis, activation of tissue lipases,
SOD, and CAT. These beneficial effects might be due
to bioactive compounds like typical alkaloids,
quinovich acid, cadambine and its derivatives present
in the root
8-10
.

Acknowledgement
One of us (V K) is grateful to Director, CDRI,
Lucknow for experimental support and Eras
Lucknow Medical college, Lucknow for financial
support.

References
1 Jain S K & DeFillps R A (1991) Anthocephalus indicus. In:
Medicinal Plants of India (Jain S K & DeFilipps, eds.),
pp 515-516, Reference Publication Inc., Algonac,
Michigan, USA
2 Sircar N N (1992) Pharmacological basis of Ayurvedic
therapy. In: Cultivation and Utilization of Medicinal Plants
(Atal C K & Kapoor B M, eds.), pp 507-518, Publication and
Information Directorate, CSIR, New Delhi, India
3 Brown R T, Fraser S B & Banerji J (1974) Tetrahedron Lett
29, 3335L
4 Brown R T & Chapple C L (1976) Tetrahedron Lett 31,
2723-2724
5 Sahu N P, Mahto S B, Banerji N & Chakravarti R N (1974)
Indian J Chem 17, 284-286
6 Chandra O & Gupta D (1980) Carbohydrate Res 83, 85-92
7 Paranjpe P (2001) Indian Medicinal Plants, Forgotten
Healers. In: A guide to Ayurvedic Herbal Medicine
(Paranjpe P, ed.), pp 112-113, Chaukhamba Sanskrit
Pratishthan, Delhi, India
8 Kumar V, Khanna A K, Khan M M, Singh R, Singh S,
Chander R, Mahdi F, Saxena J K, Saxena S, Singh V K &
Singh R K (2009) Indian J Clin Biochem 24, 65-69
9 Kumar V, Khan M M, Khanna A K ,Singh R , Mahdi F,
Manhdi A A, Saxena J K & Singh R K (2008) Evid Based
Complement Altern Med DOI: 10.1093/ecam/ nen001
10 Kumar V, Singh S, Khanna A K, Khan M M, Chander R,
Mahdi F, Saxena J K, Singh R & Singh R K (2008) Med
Chem Res 17, 152-158
11 Nagappa A N, Thakurdesai P A, Venkat Rao N & Singh J
(2003) J Ethnopharmacol 88, 45-50
12 Adewole S O & Ojewole J A (2006) Pharmacologyonline l,
120-134
13 Ceriello A (2000) Metabolism 49, 27-29
14 Wolf S P & Dean R T (1987) Biochem J 245, 243-250
15 Halliwell B & Gutteridge J M (1990) Meth Enzymol 186,
1-85
16 Baynes J W & Thrope S R (1999) Diabetes 48, 1-9
KUMAR et al.: HYPOLIPIDEMIC AND ANTI-OXIDATIVE EFFECT OF ANTHOCEPHALUS INDICUS ROOT


109
17 Satyanarayan T, Katyayani B M, Hema L E, Mathews A A &
China E M (2006) Pchog Mag 2, 244-253
18 Lavhale M S & Mishra S H (2007) Indian J Exp Biol 45,
376-384
19 Stanely Mainzen P P, Kamalakkannan N & Venugopal P M
(2004) J Ethnopharmacol 91, 209-213
20 Pavana P, Sethupathy S & Manoharan S (2007) Indian J
Clin Biochem 22, 77-83
21 Burstein M & Legmann P (1982) Lipoprotein Precipitation.
In: Monographs on Atherosclerosis (Clarkson T B, ed.),
pp 78-93, S Karger, London, Paris, New York.
22 Zlatkis A Zak B & Boyle A J (1953) J Lab Clin Med 41,
486-492
23 Van Handel S E & Zilversmit D B (1957) J Lab Clin Med
50, 152-157
24 Zilversmit D B, Davis A K, Memphis B & Tenn N (1950)
J Lab Clin Med 35, 155-160
25 Chander R, Singh C & Kapoor N K (1988) Life Sci Adv
7,25-27
26 Ohkawa H, Ohisha N & Yagi K(1979) Anal Biochem 95,
351-360
27 Mosinger F (1965) J Lipid Res 6, 157-159
28 Lowery O H, Rosen Brough N J, Fars A L & Randall R J
(1951) J Biol Chem 193, 265-75
29 Nagasaki T & Akanuma Y (1977) Clin Chem Acta 75,
371-375
30 Wing D R & Robinson D (1968) Biochem J 109, 841-849
31 Mayes PA & Felts J M (1968) Biochem J 108, 483-487
32 McCord J M & Fridovich I J (1969) Biol Chem 244,
6049-6055
33 Aebi H, Heiniger J P & Lanber E (1974) Helv Chim Acta
47, 1428
34 Mosbach E H, Klenisky H J, Hal P, Kendall F E (1954) Arch
Biochem Biophys 51, 402-409
35 Woodson R F (1957) Statistical Methods for the Analysis of
Biochemistry Data, p 315, Chichester Wiley, England
36 Tyrberg B, Anderson A & Borg L (2001) Gen Comp
Endocrinol 122, 238-251
37 Sharma N & Garg V (2009) Indian J Biochem Biophys 46,
99-105
38 Nikila E A (1971) Progr Biochem Pharmacol. 6, 102-129
39 Elkeles R S and Hambley J (1977 Diabetes, 26, 58-60
40 Ballantyne C M, Herd J A, Feriic L L, Dunn J K, Farmer J A,
Jones P H, Scheim J R & Gotto A M Jr. (1999) Circulation
90, 736-743
41 Stanley Mainzen Prince P, Venugopal P. Menon &
Gunasekaran G (1999) Ethnopharmacol 64, 53-57
42 Khanna A K, Rizvi F & Chander R (2002)
J Ethnopharmacol 82, 19-22
43 Seidel D & Wall A (1983) Lecithin Cholesterol Acyl
Transferase. In: Liver in Metabolic Diseases (Landman L &
Staddler G A, eds.), pp 81-95, MIP Press, Lancaster, England