Experimental and Toxicologic Pathology 64 (2012) 75–79

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Experimental and Toxicologic Pathology

journal homepage: www.elsevier.de/etp

Antidiabetic, antihyperlipidemic and antioxidant activities of methanolic extract

of Amaranthus viridis Linn in alloxan induced diabetic rats
B.S. Ashok Kumar a,∗ , K. Lakshman b , K.N. Jayaveea c , D. Sheshadri Shekar d , Saleemulla Khan e ,
B.S. Thippeswamy f , Veeresh P. Veerapur g
a
Department of Pharmacognosy, Sri K.V. College of Pharmacy, M.G. Road, Chickballapur, Karnataka 562101, India
b
Department of Pharmacognosy, PES College of Pharmacy, Bangalore, Karnataka, India
c
Department of Chemistry, Jawaharlal Nehru Technological University, College of Engineering, Anantapur, Andhra Pradesh, India
d
Department of Pharmacology, Sri K.V. College of Pharmacy, Chickballapur, Karnataka 562101, India
e
Department of Pharmacognosy, Manipal College of Pharmaceutical Sciences, Manipal, Karnataka, India
f
Department of Pharmacology, Sree Siddhaganga College of Pharmacy, Tumkur, Karnataka, India
g
Department of Quality Assurance, Sree Siddhaganga College of Pharmacy, Tumkur, Karnataka, India

a r t i c l e i n f o a b s t r a c t

Article history: The aim of this study was to investigate the antidiabetic, antihyperlipidemic and antioxidant activities
Received 19 March 2010 of methanolic extract of whole plant of Amaranthus viridis (MEAV) in alloxan (ALX) induced diabetic
Accepted 11 June 2010 rats. Diabetes was confirmed after 5 days of single intraperitoneal injection of ALX (140 mg/kg) in albino
Wister rats. MEAV (200 and 400 mg/kg) and glibenclamide (10 mg/kg, p.o.) orally administered daily for
Keywords: 15 days, blood was withdrawn for glucose determination on 0, 1, 10 and 15 days respectively. On the
Amaranthus viridis Linn
15th day, overnight fasted rats were sacrificed and blood was collected for the determination of high
Alloxan
density lipoproteins cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), very low density
Antidiabetic
Antihyperlipidemic
lipoprotein cholesterol (VLDL-C), total cholesterol (TC), total glycerides (TG) and total proteins (TP). For
Antioxidants in vivo antioxidant activity of MEAV, liver tissues were homogenized and the assay of lipid peroxidation
In vitro ␣-amylase inhibition and was measured as Malondialdehyde (MDA), glutathione (GSH), catalase (CAT) and total thiols (TT)
were performed in control, ALX and MEAV treated rats. MEAV at doses of 200 and 400 mg/kg showed
significant reduction is blood glucose, lipid profiles and significant improvement in MDA, GSH, CAT and
TT when compared to diabetic control group. In vitro ␣-amylase inhibition activity of MEAV was also
studied. We concluded that MEAV possess antidiabetic, antihyperlipidemic and antioxidant activities.
© 2010 Elsevier GmbH. All rights reserved.

1. Introduction exerts its diabetogenic actions when administered intravenously,

The worldwide epidemic of type 2 diabetes (NIDDM) has been
stimulating the search for new concepts and targets for the treat-
ment of this incurable disease. Globally diabetes has shadowed the
spread of modern lifestyle and it can be linked to an increase over-
weight and sedentary population (Vats et al., 2003). Hyperglycemia
and hyperlipidemia are two important characters of diabetes mel-
litus, an endocrine based disease. Diabetic patients experience
various vascular complications, such as atherosclerosis, diabetic
nephropathy and neuropathy (Sheetz, 2002). It is now well estab-
lished that the hyperlipidemia represents a major risk factor for the
premature development of atherosclerosis and its cardiovascular
complications (Goldstein et al., 1973; Kaur et al., 2002).
Alloxan (2,4,5,6-tetraoxypyrimidine; 5,6-dioxyruacil) has been
commonly utilized as an animal model of diabetes. Alloxan
∗ Corresponding author.
E-mail address: ashok4vani@gmail.com (B.S. Ashok Kumar).
intraperitoneal or subcutaneously. The action of alloxan in the
pancreas is preceded by its rapid uptake by the insulin-secreting
cells (␤-cells) (Heikkila et al., 1976), and also due to autoimmune
destruction of the ␤-cells of the pancreas (Atkinson and Maclaren,
1994).
Over the years, various medicinal plants and their extracts
have been reported to be effective in the treatment of dia-
betes (Marles and Fransworth, 1995). Plants are rich sources of
antidiabetic, antihyperlipedemic and antioxidant agents such as
flavonoids, gallotannins, amino acids and other related polyphenols
(Muruganandan et al., 2005; Miyake et al., 2006).
Amaranthus viridis L. (Amaranthaceae) commonly called as
‘Chilaka Thota-Kura’ in Telugu. A. viridis has been used in Indian tra-
ditional system and in Nepal to lesson labour pain and as antipyretic
(Kirtikar and Basu, 1987; Mark and Turin, 2003). The Negritos of
the Philippines apply the bruised leaves directly to eczema, pso-
riasis and rashes (Quisumbing, 1951). Other traditional uses are
anti-inflammatory of the urinary tract, in venereal diseases, ver-
mifuge, diuretic, antirheumatic, antiulcer, analgesic, antiemetic,

0940-2993/$ – see front matter © 2010 Elsevier GmbH. All rights reserved.
doi:10.1016/j.etp.2010.06.009
76 B.S. Ashok Kumar et al. / Experimental and Toxicologic Pathology 64 (2012) 75–79
laxative, improves appetite, antileprotic, respiratory problems, eye
treatment and for asthma (Anonymous, 1988; Agra et al., 2007;
De Fatima Agra et al., 2008; Kirtikar and Basu, 1987; Sher and
Khan, 2006; Quershi et al., 2008; Dar, 2003; Arshad and Khan, 2000;
Muhammad and Amusa, 2005). A novel antiproliferative, antifun-
gal lectin, ribosome inactivating protein, ␤-carotene were isolated
from A. viridis (Kaur et al., 2006; Kwon et al., 1997; Sena et al., 1998)
and it possess antiviral activity (Obi et al., 2006). In the present
study, we have evaluated the antidiabetic, antihyperlipedemic and
antioxidant activities of methanol extract of whole plant of A. viridis
linn.
2. Materials and methods
2.1. Collection of plant material and extraction
The fresh plant of A. viridis was collected from Chickballapur
and was authenticated by Prof. B.K. Venkatesh, Department of
Botany, Government First grade College, Chickballapur (Karnataka).
A voucher specimen (SKVCP 11) was deposited in college herbar-
ium. The whole plant was shade dried and coarsely powdered. The
coarse powder was subjected to extraction with methanol by soxh-
let apparatus and extract was concentrated to dryness in vacuum.
The greenish brown extract was obtained and is dissolved in Tween
80 of pharmacological studies.
2.2. Preliminary phytochemical screening
The methanol extract of A. viridis was screened for the presence
of various phytoconstituents like steroids, alkaloids, glycosides,
flavonoids, carbohydrates, amino acids, proteins and phenolic com-
pounds (Kokate, 1986).
2.3. Animals
Male Swiss Albino Wistar rats weighing 150–250 g were accli-
matized to the experimental room at temperature 23 ± 2 ◦ C,
controlled humidity conditions (50–55%) and 12 h light and dark
cycle. They were caged with a maximum of two animals in
polypropylene cage and were fed with standard food pellets
(Kamadenu Enterprises, Bangalore) and water ad libitum. All the
studies conducted were approved by the institutional animal ethi-
cal committee of Sri K.V. College of Pharmacy (Reg. No. 117/2000),
Chickballapur, Karnataka, according to prescribed guidelines of
CPCSEA, Government of India.
2.4. Induction of diabetes
The animals were fasted for 12 h prior to the induction of
diabetes as described by Joy and Kuttan (1999) with slight mod-
ification. ALX freshly prepared in 0.5% Tween 80 was administered
intraperitoneally (i.p.) at single dose of 140 mg/kg. Development of
diabetes was confirmed by measuring blood glucose concentration
5 days after the administration of ALX. Rats with blood glucose level
of above 200 mg/dl were considered to be diabetic and used for the
studies.
2.5. Experimental design
The rats were randomized into five groups comprising of six
animals in each groups as given below. Solvent/MEAV (200 and
400 mg/kg)/glibenclamide (GLB) was administered orally using an
intra-gastric tube once daily for 15 days.
• Group I: normal control rats, received 0.5% Tween 80.
• Group II: diabetic control received ALX in single dose (140 mg/kg.
i.p.).
• Group III: diabetic rats received MEAV (200 mg/kg/day. p.o.), 5
days after ALX treatment.
• Group IV: diabetic rats received MEAV (400 mg/kg/day. p.o.), 5
days after ALX treatment.
• Group V: diabetic rats received with GLB (10 mg/kg/day, p.o.), 5
days after ALX treatment.
Blood samples were collected from retro-orbital plexus of each
rat under mild anesthesia at 0, 1, 2 and 3 h after solvent/MEAV (200
and 400 mg/kg)/GLB administration and serum glucose was esti-
mated by enzymatic glucose oxidase method. Percent reduction in
serum glucose was calculated with respect to the initial level.
Five days before the termination of the experiment, the oral glu-
cose tolerance test (OGTT) was performed to assess the glucose
tolerance. For this purpose, overnight fasted rats were fed glucose
(2 g/kg) orally and blood was collected at 0, 30, 60 and 120 min
interval from orbital sinus for glucose estimation. On 15th day of
the study, blood samples were collected for biochemical estima-
tions. Later animals were sacrificed and liver was removed, cleaned
and washed in ice-cold normal saline for biochemical study.
2.6. Biochemical analysis
Serum total cholesterol (Demacker et al., 1980), total glycerides
(Foster and Dunn, 1973), LDL-c, VLDL-c (Friedwald et al., 1972)
and HDL-c (Assmann et al., 1983) were estimated using standard
enzymatic kits (ERBA diagnostic Mannheim GMBH, Germany) spec-
trometrically. Total protein was estimated by the method of Lowery
et al. (1951) using bovine serum albumin as a standard. Lipid per-
oxidation was measured as malondialdehyde (MDA) (Gelvan and
Saltman, 1990). GSH was determined according to the method of
Moran et al. (1979), CAT activity was determined according the
method of Claiborne (1985) and TT was determined according to
the method of Moran et al. (1979).
2.7. In vitro ˛-amylase inhibition assay of MEAV
The ␣-amylase inhibitory activity for MEAV was determined
based on the spectrophotometric assay using acarbose as the ref-
erence compound (Gella et al., 1997). The MEAV was dissolved
in DMSO to give concentrations from 10, 50 and 100 ␮g/ml. The
enzyme ␣-amylase solution (0.5 unit/ml) was prepared by mixing
3.246 mg of ␣-amylase (EC 3.2.1.1) in 100 ml of 40 mM phosphate
buffer pH 6.9. Add 60 ␮l of 40 mM phosphate buffer (pH 6.9)/acar-
bose/MEAV and 30 ␮l of ␣-amylase enzyme are preincubated at
37 ◦ C for 10 min and then 120 ␮l of 2-chloro-p-nitrophenyl-␣-d-
maltotrioside (CNPG3) was added, mixed and incubated at 37 ◦ C
for 8 min. The absorbance was measured at 405 nm and control
reaction was carried out without the extract. Percentage inhibition
was calculated by expression:
AbsorbanceControl − AbsorbanceTest
% Inhibition = × 100
AbsorbanceControl
2.8. Statistical analysis
Results were expressed as the mean ± S.E.M. for statistical
analysis of the data group means, were compared by one-way
analysis of variance (ANOVA) followed by Tukey’s post-test for
multiple comparisons. p < 0.001 was considered to be statistically
significant.
 B.S. Ashok Kumar et al. / Experimental and Toxicologic Pathology 64 (2012) 75–79 77

Fig. 1. Effect of single dose treatment of MEAV on blood glucose level in diabetic
rats. The percentage reduction in glycaemia with respect to the initial (0 h) level.
Each value represents mean ± S.E.M., n = 6. *p < 0.05, ***p < 0.001 compared to dia-
betic control of the same time interval. MEAV = methanolic extract of A. viridis and
GLB = glibenclamide.
Fig. 2. Effect of MEAV on oral glucose tolerance in normal and ALX-induced dia-
betic rats. Each value represents mean ± S.E.M., n = 6. ***p < 0.001 compared to
diabetic control of the same time interval. MEAV = methanolic extract of A. viridis
and GLB = glibenclamide.

3.3. Antihyperlipidemia effect of MEAV

3. Results
3.1. Preliminary phytochemical screening
By preliminary phytochemical analysis of MEAV showed
the presence of flavonoids, saponins, glycosides, terpenoids
aminoacids, alkaloids, carbohydrates, phenolic compounds and
proteins.
ALX treatment resulted in significant (p < 0.001) elevation of TG,
TC, VLDL-C, LDL-C, and reduction of HDL-C levels as compared to the
normal control rats. MEAV (200 and 400 mg/kg) and GLB (10 mg/kg)
significant (p < 0.001) reduction in elevated TG, TC, VLDL-c, LDL-c,
TC/HDL-c and LDL-c/HDL-c and HDL-c level was restored respec-
tively when compared to diabetic control (Table 2).
3.4. Antioxidant activity of MEAV

3.2. Antidiabetic effect of MEAV

Table 3 shows the effect of administration of MEAV on MDA,
GSH, CAT, TT and TP in liver tissue of different groups of rats.
Fig. 1 reveals that the effect of MEAV on blood glucose level of
There was significant (p < 0.001) elevation in tissue MDA in dia-
diabetic rats during single dose study. MEAV (200 and 400 mg/kg)
betic rats as compared to normal rats. Treatment with MEAV for 15
and glibenclamide (10 mg/kg) were given orally to the different
days resulted in significant (p < 0.001) decrease in liver tissue MDA.
groups and showed significant (p < 0.001) percentage reduction in
GSH, CAT and TT contents in diabetic control rats were significantly
glycemia when initial value of same group.
(p < 0.001) depleted in liver tissue when compared with normal
Fig. 2 reveals the effect of MEAV on glucose tolerance test. MEAV
rats. MEAV treatment at both dose levels significantly (p < 0.001)
(200 and 400 mg/kg) and glibenclamide (10 mg/kg) were showed
restored GSH, CAT and TT and (p < 0.01) TP levels as compared with
significant (p < 0.001) reduction in blood glucose level was observed
diabetic control.
after 2 h of glucose administration when compared to diabetic con-
trol.
Table 1 shows the effect of MEAV on blood glucose levels of dia- 3.5. In vitro ˛-amylase inhibition assay of MEAV
betic and animals after the daily treatment (200 and 400 mg/kg) for
15 days. Showed significant (p < 0.001) percentage fall in blood glu- Table 4 results revealed that MEAV showed significant inhibition
cose levels with the doses of 200, 400 mg/kg of MEAV and 10 mg/kg of ␣-amylase enzyme. IC50 values of MEAV and acarbose are 10.19
of GLB as compared to diabetic control group. and 0.312 ␮g/ml respectively.

Table 1
Effect of methanolic extract of Amaranthus viridis on blood glucose level in ALX-induced diabetic rats.

Groups Treatment Blood glucose level (mg/dl)

0 day 1st day 10th day 15th day

I Control 86.75 ± 2.18 87.44 ± 2.34 62.66 ± 5.6 84.98 ± 3.8

II Diabetic control (DC) 316.84 ± 47.13 354.74 ± 39.98 378.94 ± 7.05 342.83 ± 40.06
III DC + MEAV (200 mg/kg) 259.7 ± 27.9 221.1 ± 41.9* 89.84 ± 9.01*** 108.4 ± 7***
IV DC + MEAV (400 mg/kg) 248.6 ± 31.4 138.3 ± 4.7*** 81.26 ± 6.86*** 95.7 ± 4***
V DC + GLB (10 mg/kg) 271.7 ± 33.1 185.2 ± 14.9** 72.16 ± 7.48*** 86.6 ± 5.6***

The data are expressed in mean ± S.E.M. n = 6 in each group.

*
p < 0.05 compared with corresponding value of diabetic control animals.
**
p < 0.01 compared with corresponding value of diabetic control animals.
***
p < 0.001 compared with corresponding value of diabetic control animals.
78 B.S. Ashok Kumar et al. / Experimental and Toxicologic Pathology 64 (2012) 75–79

Table 2
Effect of methanolic extract of Amaranthus viridis on lipid profiles in ALX-induced diabetic rats.

Groups Treatment TG TC HDL-c VLDL-c LDL-c TC/HDL-c LDL-c/HDL-c

I Control 60.89 ± 3.36 64.33 ± 2.24 33.37 ± 1.36 12.18 ± 0.67 18.78 ± 2.98 1.95 ± 0.12 0.58 ± 0.10
II Diabetic control (DC) 179.44 ± 18.71# 159.84 ± 5.95# 14.47 ± 1.25# 35.89 ± 3.74# 109.48 ± 5.95# 11.55 ± 1.31# 8 ± 1.1#
III DC + MEAV (200 mg/kg) 114 ± 6.6*** 94.6 ± 6.9*** 20.8 ± 1.2*** 22.8 ± 1.3*** 50.9 ± 6.6*** 4.6 ± 0.3*** 2.5 ± 0.3***
IV DC + MEAV (400 mg/kg) 63.3 ± 4.3*** 63.7 ± 3.3*** 26.8 ± 1.3*** 12.7 ± 0.9*** 24.2 ± 3.7*** 2.4 ± 0.2*** 0.9 ± 0.2***
V DC + GLB (10 mg/kg) 62.7 ± 2.9*** 71.8 ± 4.7*** 27.6 ± 1.4*** 12.5 ± 0.6*** 31.7 ± 5.5*** 2.7 ± 0.3*** 1.2 ± 0.3***

The data are expressed in mean ± S.E.M. n = 6 in each group.

***
p < 0.001 compared with the corresponding value for diabetic control animals.
#
p < 0.001 compared with the corresponding value for the normal control animals.

Table 3
Effect of methanolic extract of Amaranthus viridis on MDA, GSH, CAT, TT and TP levels in ALX-induced diabetic rats.

Treatment MDA (nmoles/g of tissue) GSH (nmoles/mg of protein) CAT (U/mg of protein) TT (␮moles/mg of protein) TP (mg/g of tissue)

Normal control 11.22 ± 0.65**

48.21 ± 2.05 **
89.38 ± 2.53**
3.92 ± 0.094 **
11.61 ± 0.53***
Diabetes control (DC) 60.76 ± 3.3# 16.26 ± 1.98# 24.28 ± 2.94# 0.6 ± 0.088# 37.67 ± 1.14
DC + MEAV (200 mg/kg) 40.26 ± 2.12*** 25.28 ± 1.26* 37.09 ± 2.03** 2.1 ± 0.19*** 36.04 ± 0.55
DC + MEAV (400 mg/kg) 27.89 ± 2.46*** 33.47 ± 2.18*** 53.94 ± 2.16*** 2.6 ± 0.12*** 32.48 ± 1.41*
DC + GLB (10 mg/kg) 19.75 ± 1.84** 39.85 ± 1.74*** 67.18 ± 2.45** 3.1 ± 0.27** 22.1 ± 1.24***

The data are expressed in mean ± S.E.M. n = 6 in each group.

MDA, malondialdehyde; GSH, glutathione; CAT, catalase; TT, total thiols; TP, total protein.
*
p < 0.05 compared with diabetic control rats.
**
p < 0.01 compared with diabetic control rats.
***
p < 0.001 compared with diabetic control rats.
#
p < 0.001 compared with normal control animals.

Table 4 cesses, which in turn leads to accumulation of lipids such TG and

In vitro ␣-amylase inhibition activity of methanolic extract of Amaranthus viridis.
Sample Concentration (␮g/ml) % inhibition
0.1 31.53 ± 0.14
Acarbose 0.5 72.49 ± 0.09
1.0 82.92 ± 0.12
10 46.34 ± 0.2
MEAV 50 68.02 ± 0.18
100 73.14 ± 0.11
The data are expressed in mean ± S.E.M. n = 3 in each group.
4. Discussion
Oxidative stress, altered lipid levels, and disturbances in glucose
metabolism are important risk factors for diabetes, cardiovascu-
lar, oncologic and many other diseases. Diet undoubtedly plays a
key role as chemopreventive agent against various diseases and
optimizing the diet in both quality and quantity, has a preventive
function. Fruit and vegetables are an invaluable source of many bio-
logically active substances, including antioxidants. For this reason a
diet rich in fruit and vegetable has a positive effect on reducing the
incidence of these serious lifestyle diseases (Van Der Schouw et al.,
2005). A. viridis, is used as vegetable, possess a wide ethnomedical
history (Kirtikar and Basu, 1987).
The diabetogenic agent alloxan is a hydrophilic and chemically
unstable pyrimidine derivative, which is toxic to pancreatic ␤-cells
because it can generate toxic free oxygen radicals during redox
cycling in the presence of reducing agents such as glutathione and
cysteine (Szkudelski, 2001). The increase in oxygen free radicals in
diabetes could be due to increase in blood glucose levels, which
generates free radicals due to autooxidation (Yadav et al., 2000).
In the present work, involvement of free radicals in progression
of disease and protective effects of A. viridis has been examined.
Administration of MEAV for 15 days showed significant antidia-
betic, antihyperlipidemic and antioxidant activities in ALX-induced
diabetic rats.
Hyperlipidemia is one of the major cardiovascular risk factors. It
has been demonstrated that insulin deficiency in diabetes mellitus
leads to a variety of derangements in metabolic and regulatory pro-
TC in diabetic patients (Goldberg, 1981). Our data were in line with
IC50 (␮g/ml) notion as the ALX (140 mg/kg, i.p.) treated diabetic rats exhibited
clear cut abnormalities in lipid metabolism as evidenced from the
0.312 significant elevation of serum TG, TC, LDL-c, VLDL-c and reduction
of HDL-C levels. Treatment with MEAV for 15 days was sufficient
to produce a significant reduction in the TG, TC, LDL-c, VLDL-c and
10.19 significant increase in HDL-c levels in diabetic rats. These results
indicate that MEAV has a lipid lowering effect on the diabetic rats.
Elevation of LPO is attributed to the enhanced production of
reactive oxygen species. In the present study, we observed a
MDA formation, the index of lipid peroxidation, was significantly
increased in liver of ALX treated animals. MEAV supplementation
potentially reduced MDA level, suggesting that MEAV might have
antioxidant principles to produce such response.
GSH protect the cellular system against the toxic effects of lipid
peroxidation. A marked depletion in the GSH content a liver was
observed in diabetic control rats (Table 3). Furthermore, MEAV
treatment showed a significant restoration in GSH content of dia-
betic rats.
The present data indicate that ALX-induced diabetes disrupts
actions of antioxidant enzymes. The decreased activities of these
enzymes may be due to the production of reactive oxygen species
(ROS) such of superoxide (O2 −• ), hydrogen peroxide (H2 O2 ), and
hydroxyl radical (OH) that reduces the activity of these enzymes
(Kaleem et al., 2005; Vincent et al., 2004). In the present study,
MEAV potentiated the enzymatic and non-enzymatic antioxidant
activities.
Drugs that inhibit carbohydrate hydrolyzing enzymes have
been demonstrated to decrease postprandial hyperglycemia and
improve impaired glucose metabolism without promoting insulin
secretion of NIDDM patients. The results of in vitro studies showed
that MEAV inhibits ␣-amylase activity. Natural health products of
vegetable origin were clearly indicated as a promising avenue for
the prevention of chronic diseases (Punitha and Manoharan, 2006).
The findings of the present study shows a number of positive
effects of A. viridis on rats with ALX-induced disturbances in glu-
cose tolerance, lipoprotein profile, and antioxidant status. Thus,
MEAV is beneficial in the control of diabetes, abnormalities in lipid
profiles and oxidative stress by activation of enzymatic and non-
 B.S. Ashok Kumar et al. / Experimental and Toxicologic Pathology 64 (2012) 75–79
enzymatic antioxidants. These beneficial effects of A. viridis are
especially promising in the light of preventing lifestyle diseases of
the cardiovascular system (Despres et al., 2000).
In conclusion, the result of the present study indicates that A.
viridis may have active principle(s) that exerts antidiabetic, anti-
hyperlipidemic and ␣-amylase activities. However, more efforts
are still needed for the isolation, characterization and biological
evaluation of the active principle(s) of the A. viridis extract.
Acknowledgments
The authors are thankful to Sri K.V. Naveen Kiran, Chairman,
Sri K.V. College of Pharmacy, Chickballapur, Karnataka (India) for
providing facilities to carry out the research work.
References
Agra MF, Baracho GS, Nurit K, Basilio IJLD, Coelho VPM. Medicinal and poi-
sonous diversity of the flora of “Cariri Paraibano” Brazil. J Ethnopharmacol
2007;111:283–395.
Anonymous. The wealth of India. A dictionary of Indian raw materials and industrial
products, vol. 1. New Delhi, India: Council of Scientific and Industrial Research
(CSIR), Publications and Information Directorate; 1988. p. 221.
Arshad M, Khan QUA. Ethnobotonical study of some medicinal plants of Rawal Town.
Pak J Biol Sci 2000;3(8):1245–6.
Assmann G, Schriewer H, Schmitz G, Hagele EO. Quantification of high density
lipoprotein cholesterol by precipitation with phosphotungstic acid/MgCl2 . Clin
Chem 1983;29:2026–30.
Atkinson MA, Maclaren NK. The pathogenesis of insulin-dependent diabetes melli-
tus. N Engl J Med 1994;24:1428–36.
Claiborne A. Handbook of methods for oxygen radical research. London: CRC Press;
1985. p. 283–4.
Dar MEI. Ethnobotonical uses of plants of Lawat district Muzaffarabad Azad Jammu
and Kashmir. Asian J Plant Sci 2003;2(9):680–2.
De Fatima Agra M, Silva KN, Basilio IJLD, De Freitas PF, Filho JMB. Survey of
medicinal plants used in the region northeast of Brazil. Braz J Pharmacogn
2008;18(3):472–508.
Demacker PN, Hijmans AG, Vos-Jansses HE, Van’t Laar A, Jansen AP. A study of the
use of polyethylene glycol in estimating cholesterol in high density lipoproteins.
Clin Chem 1980;26:1775–9.
Despres JP, Lemieux I, Dagenais GR, Cantin B, Lamarche B. HDL-cholesterol as a
marker of coronary heart disease risk: the Quebec cardiovascular study. Ather-
scler 2000;153:263–72.
Foster JB, Dunn RT. Stable reagents for determination of serum triglyceride by col-
orimetric condensation method. Clin Chem Acta 1973;19:338–40.
Friedwald J, Levy YR, Friedrickson SD. Estimation of concentration of low density
lipoprotein cholesterol in plasma without use of preparative ultracentrifuge.
Clin Chem 1972;18:499–502.
Gella FJ, Gubern G, Vidal R, Canalias F. Determination of total and pancreatic ␣-
amylase in human serum with 2-chloro-4-nitrophenyl-␣-d-maltotrioside as
substrate. Clin Chem Acta 1997;259:147–60.
Gelvan D, Saltman P. Different cellular targets of Cu- and Fe-catalyzed oxidation
observed using a Cu-compatible thiobarbiturate acid assay. Biochem Biophys
Acta 1990;1035:353–60.
Goldberg RB. Lipid disorders in diabetes. Diabetes Care 1981;4:561–72.
Goldstein JL, Schrott HG, Hazzard WR, Bierman EL, Motulsky AG. Hyperlipidemia
in coronary heart disease 11, genetic analysis of lipid levels in 176 families and
delineation of a new inherited disorder, combined hyperlipidemia. J Clin Invest
1973;52:1544–68.
79
Heikkila RE, Winston B, Cohen G. Alloxan induced diabetes evidence for hydroxyl
radical as a cytotoxic intermediate. Biochem Pharmacol 1976;25:1085–92.
Joy KL, Kuttan R. Antidiabetic activity of Picrorrhiza kurroa extract. J Ethanopharma-
col 1999;67:143–8.
Kaleem M, Sheema, Sarmad H, Bano B. Protective effects of Piper nigrum and
Vinca rosea in alloxan induced diabetic rats. Indian J Physiol Pharmacol
2005;49:65–71.
Kaur N, Dhuna V, Kamboja SS, Agrewala JN, Singh J. A novel antiproliferative
and antifungal lactin from Amaranthus viridis Linn, seeds. Protein Pept Lett
2006;13(9):897–905.
Kaur J, Singh P, Sowers JR. Diabetes and cardiovascular diseases. Am J Ther
2002;9:510–5.
Kirtikar KR, Basu BD. Indian medicinal plants, vol. 3. Dehra Dun, India: International
Book Distributors; 1987. p. 2061–2.
Kokate CK. Preliminary phytochemical screening, practical pharmacognosy. 1st ed.
New Delhi: Vallabh Prakashan; 1986. p. 111.
Kwon SY, An CS, Liu JR, Pack KH. A ribosome inactivating protein from Amaranthus
viridis. Biosci Biotechnol Biochem 1997;61(9):1613–4.
Lowery OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin
phenol reagent. J Biol Chem 1951;193:265–75.
Mark and Turin. Ethnobotonical notes on Thangmi plant names and their medicinal
and ritual uses. CNAS J 2003;30:1.
Marles RJ, Fransworth NR. Antidiabetic plants and their active constituents. Phy-
tomedicine 1995;2:137–89.
Miyake Y, Suzuki E, Ohya S, Fukumoto S, Hirmitsu M, Sakaida K, et al. Lipid-lowering
effect of eriocitrin, the main flavonoid in lemon fruit, in rats on a high fat and
high-choletsterol diet. J Food Sci 2006;71:S633–7.
Moran A, Depierre JW, Mannervick B. Levels of glutathione, glutathione reduc-
tase, glutathione-S-transferase activities in rat liver. Biochem Biophys Acta
1979;582:67–8.
Muhammad S, Amusa NA. The important food crops and medicinal plants of north-
western Nigeria. Res J Agric Biol Sci 2005;1(3):254–60.
Muruganandan S, Srinivasa K, Gupta S, Gupta PK, Lal J. Effect of Maniferin on hyper-
glycemia and atherogenicity in streptozotociin diabetic rats. J Ethnopharamcol
2005;97:497–501.
Obi RK, Iroagba II, Ojiako OA. Virucidal potential of some edible Nigerian vegetable.
Afr J Biotechnol 2006;5(19):1785–8.
Punitha R, Manoharan S. Antihyperglycemic and antilipidperoxidative effects of
Pongamia pinnata (Linn.) Pierre flowers in alloxan induced diabetic rats. J
Ethanopharmacol 2006;105:39–46.
Quershi SJ, Khan MA, Ahmed M. A survey of useful medicinal plants of Abbottabad,
in Northern Pakistan. Trakia J Sci 2008;6(4):39–51.
Quisumbing E. Medicinal plants of the Philippines. Manila: Department of Agricul-
ture and Natural Resources, Bureau of Printing; 1951. p. 298–351.
Sena LP, Vanderjagt DJ, Rivera C, Tsin ATC, Muhamadu I, Mahamadou O, et al. Analysis
of nutritional components of eight famine foods of the Republic of Nigeria. Plant
Foods Hum Nutr 1998;52(1):17–30.
Sheetz MJ. Molecular understanding of hyperglycemias adverse effects for diabetic
complications. J Am Med Assoc 2002;288:2579–88.
Sher H, Khan ZD. Resource utilization for economic development and folk medicine
among the tribal people. Observation from northern part of Pakistan. Pak J Plant
Sci 2006;12(2):149–62.
Szkudelski T. The mechanism of Alloxan and Streptozotocin action in B cells of the
rat pancreas. Physiol Res 2001;50:537–46.
Vats RK, Kumar V, Kothari A, Mital A, Ramachandran U. Emerging targets for diabetes.
Curr Sci 2003;88:241–9.
Van Der Schouw YT, Kreijkamp-Kaspers S, Peeters PH, Keinan-Boker L, Rimm EB,
Grobbee DE. Prospective study on usual dietary phytoestrogen intake and car-
diovascular disease risk in western women. Circulation 2005;111:465–71.
Vincent AM, Russel JW, Low P, Feldman EL. Oxidative stress in the pathogenesis of
diabetic neuropathy. Endocrine Rev 2004;25:612–28.
Yadav SB, Tripathi V, Singh RK, Pandey HP. Antioxidant activity of Cuscuta reflexa
stem. Indian J Pharm Sci 2000;62:477–8.