Omar & Areeg

ISSN: 2279 - 0594
Journal of Biomedical and Pharmaceutical Research
Available Online at www.jbpr.in
CODEN: - JBPRAU (Source: - American Chemical Society)
Volume 5, Issue 2: March-April: 2016, 29-42
Research Article
*Corresponding author: Dr. Omar A. Farid.| E-mail: ebntaimya@yahoo.com
29
Developing a Herbal Cocktail for prevention of Stroke and cerebrovascular diseases
A.M. Algohary
1
, Raid Al Baradie
2
, O.A Ahmed-Farid
3
, A.M. Abd-Elrazek
4
and A.M. Al-Sulaiman
5
1
Assistant Professor, Medical laboratory Department, CAMS, Majmaah University, KSA Pharmaceutical Chemistry Department,
NODCAR, Giza, Egypt.
2
Assistant Professor, Medical laboratory Department, CAMS, Majmaah University, KSA.
3
Researcher, National Organization for Drug Control and Research (NODCAR), Giza 12553, Egypt.
4
Researcher, National Organization for Drug Control and Research (NODCAR), Giza 12553, Egypt.
5
Assistant Professor, Consultant in Molecular& Medical Virology, Alnakeel Medical Center. KSA.
Received 23 March 2016; Accepted 03 April 2016
ABSTRACT
Natural herbs have long been used in food supplements to promote health as healthy alternative to the
various conditions/diseases as preventive medicine. A variety of herbs and prescriptions have been
demonstrated to have neuroprotective effects in vivo and in vitro that may be relevant to the treatment of
stroke.
The present study carried out to investigate the development of hyperlipidemia in response to a high fat
diet (HFD) and to estimate the effect of 70% ethanolic extracts for herbal cocktail (Artemisia Judaica
50mg/kg B.wt, Panax ginseng 50mg/kg B.wt, Salvia officinalis 100mg/kg B.wt and Polygonum multiflorum
400mg/kg B.wt) on lipid profiles, oxidative stress markers, and inflammatory mediators in blood and liver
tissue in rats. The anti-hyperlipidemic and antioxidant effect of herbal cocktail were studied high fat diet
induced hyperlipidemic rats. Serum total lipid (TL), cholesterol (TC), triglycerides (TG), LDL and oxidative
stress marker (MDA, GSSG, NO and 8-OH-dG) were significantly lowered by herbal cocktail. Herbal cocktail
increased the activities of reduced glutathione (GSH) and HDL while significantly decreasing inflammatory
mediators (TNF-α, IL1-β and IL-6). It could be concluded that HFD induced hyperlipidemia associated with a
disturbed lipid profile, defective antioxidant stability, and high values of inflammatory mediators; this may
have implications for the progress of obesity related problems. Treatment with individual herb and herbal
cocktail improve obesity and its associated metabolic syndrome problems. Herbal cocktail has
hypolipidaemic and antioxidant effects. Moreover, herbal cocktail might be a safe combination on the
organs whose functions were examined, as a way to surmount the obesity state; and it has a distinct anti-
obesity effect.
Keywords: Artemisia Judaica, Panax ginseng, Salvia officinalis, Polygonum multiflorum, Antiobesity and High
fat diet.
INTRODUCTION:
Stroke is one of the leading causes of death. About
600,000 people experience a first-time stroke every
year. Stroke ranks number three among all causes of
death, after heart disease and cancer. Incidence of
stroke has decreased between 1950 and 2004 from
7.6% in men and 6.2%in women (1950–1977) to 5.3% in
men and 5.1% in women (1990–2004) [1]. Major
modifiable risk factor for stroke is hyperlipidemia.
Dyslipidemia has long been recognized as a risk factor
for coronary artery disease, but its role in stroke has
become increasingly apparent over the past decade.
Hyperlipidemia is a condition associated with increased
level of lipids in plasma leading to various disorders
including coronary artery disease. Hyperlipidemia is a
highly predictive risk factor for atherosclerosis,
coronary artery disease and cerebrovascular disease
[2]. In recent years, cardiovascular diseases such
Atherosclerosis, that are caused as a result of
hyperlipidemia elevate mortality percent, and the age
of death has reduced, so reducing serum
hyperlipidemia is very important; a 1% reduction in
serum cholesterol concentration results in a 2%
reduction in the prevalence of coronary artery diseases
[3]. It is clearly established that long-term consumption
of a high fat diet accelerates the development of
Coronary Heart Disease (CHD). Dietary cholesterol can

Dr. Omar A. Farid.et al., Journal of Biomedical and Pharmaceutical Research
© 2016 All Rights Reserved. CODEN (USA): JBPRAU
30
increase the level of serum cholesterol to levels which
can place an individual at increased risk for the
development or exacerbation of atherosclerosis [4].
Coronary Heart Disease (CHD) increases dramatically as
the plasma concentration of LDL cholesterol increases.
The approach of reducing dietary cholesterol suffers
from two limitations, the first is that cholesterol is
present in all animal fats and many people are unwilling
to scarify their preferred diet. The second is that the
liver and other tissues synthesize cholesterol de novo if
the dietary supply is inadequate. Consequently, the
development of methods for lowering LDL cholesterol
levels has become a major focus of medical research. In
recent years, many synthetic drugs have been used to
treat cardiac problems. These drugs produce different
side effects, depending on their mechanisms of action
which may lead to severe complications [5]. Hence
present trend is diverting towards the screening of
traditional herbal medicines to treat fatal diseases. The
use of herbal medicine has become more prevalent,
and the past few decades have witnessed a rapidly
increasing demand worldwide. The range of medicinal
plants is very diverse and it has been estimated that
around 70,000 different plant species have been used
at least once during the history of traditional medicine
[6].
Artemisia genus (Asteraceae, Anthemideae,
Artmisiianae) comprises hundreds (about 500) of
different species, but its systematic classification
remains discussed. In general five different subtaxa are
considered [7]. Artemisia have biological activates,
including the inhibition of aflatoxin B1 bio-
transformation to aflatoxin B1 [8] and potent
protection effects on CCl4 induced acute hepatotoxicity
in rats [9].
Won-Sik et al., (2013) [10] showed that the ethanolic
extract of Artemisia decrease cholesterol level for male
SpragueDawley rats fed a high-fat diet (HFD) for 4 wk.
Ginseng is known to affect various tissues including
nervous, cardiovascular, endocrine, and immune
system tissues; its major physiologically active
ingredients include ginsenosides, polysaccharides,
amino acids, polyacetylenes, alkaloids, and phenolic
compounds [11]. A major class of active compounds
related to the physiological activity of ginseng is the
ginsenosides, which are divided into dammarane type
and oleanane type, depending on the binding sugar
moiety; research studies on ginseng have mainly
studied the efficacy of saponins such as ginsenoside,
although ginseng saponins have been reported to have
relatively low antioxidant effects [12]. According to
recent studies, a hypolipidemic effect of Panax ginseng
extract (PGE) is associated with decrease in total
cholesterol (TC), triglycerides (TGs), low-density
lipoprotein (LDL), Muscular Dystrophy Association
(MDA) levels and an increase in high-density lipoprotein
(HDL) level. Administration of PGE increased serum
superoxide dismutase (SOD) and catalase (CAT)
activities while decreased MDA level indicating that
antioxidant potential of PGE might induce
hypolipidemic effect as one of action mechanism [13].
Salvia officinalis L. is a spice, popularly known as sage
that belongs to the Lamiaceae family [14]. In folk
medicine, the leaves are mainly used, but the flowers
and stems have also been used in infusions and
alcoholic extracts for various therapeutic purposes.
Sage leaf contains tannic acid, oleic acid, ursonic acid,
ursolic acid, niacin, nicotinamide, flavones, flavonoid
glycosides, cornsole, cornsolic acid, fumaric acid,
chlorogenic acid, caffeic acid, and estrogenic substances
[15]. Investigations have taken place into using sage as
a treatment for hyperlipidemia and Alzheimer’s disease
[16]. Antioxidants affect blood sugar and antioxidant
properties of Salvia officinalis L (Sage) leaves are known
[17]. Polygonum extracts exhibited anti-obesity effects
by suppressing lipogenesis in white adipose tissue and
increasing antioxidant activity. Besides, its low toxicity
in mice and its historical use suggested PE might be
used as a safe anti-hyperlipidemia pharmaceutical [18].
Plasma cholesterol, plasma triglyceride and low-density
lipoprotein cholesterol increased, while very low-
density lipoprotein cholesterol attenuated after
treatment with a water-soluble fraction of Polygonum
multiflorum (PM), suggesting PM might be applicable
for the treatment of hyperlipidemia disease [19]. In a
high fat/cholesterol rabbit model, polydatin from
Polygonum cuspidatum obviously decreased the serum
levels of total cholesterol (TC), triglyceride (TG), and
low-density lipoprotein cholesterol. Meanwhile, the
ratio of TC and the liver coefficient were also reduced
[20].
Herbal mixture seemed to be beneficial for the
reduction of body weight and improvement of
antioxidant status of the erythrocytes, and its anti-
hyperlipidemic property was highly active for enhancing
the profile of plasma lipids in rats.
Therefore, the aim of this study was to evaluate
possible effects of different herbal cocktail on serum
lipid profile, inflammatory mediators and liver oxidative
stress marker of male rat which may reflect a specific
allowances being a critical obstacle for Stroke and
cerebrovascular diseases.
Material and methods
This study was carried out at animal physiology Lab.,
NODACR, Giza, Egypt starting from the first of July till
the end of September 2015.
Extract preparation:

31
Approximately 150 g of Artemisia Judaica leaf were
extracted twice with 70% ethanol using a 2 h reflux
extraction, and the extract was concentrated under
reduced pressure. The concentrate was filtered,
lyophilized, and subsequently stored at 4∘C. The yield
of the dried extract from starting crude materials was
16.22% (w/w).
Approximately 100 g of Panax ginseng root were
extracted twice with boiling water, filtered, evaporated
in a rotary vacuum evaporator, and freeze-dried. The
yield of the dried extract from starting crude materials
was 21.07% (w/w).
Approximately 200 g of Salvia officinalis leaf were
extracted twice with 70% ethanol using a 2 h reflux
extraction, and the extract was concentrated under
reduced pressure. The concentrate was filtered,
18.81% (w/w).
Approximately 1500 g of Polygonum multiflorum root
were extracted twice with 70% ethanol using a 2 h
reflux extraction, and the extract was concentrated
under reduced pressure. The concentrate was filtered,
13.73% (w/w).
1. Experimental design
A total of ninety six rats (Sprague Dawley) were utilized
in this study. The rats had an initial weight 200±20 g (9-
12 weeks old). Rats were randomly divided into sixteen
groups, each comprising six rats. The study was
conducted for three months which included 60 days of
feeding period and next 30 days of treatment period.
Group I served as normal control was fed with standard
rat chow throughout the study. Group II to VII were fed
with high-fat diet for 60 days during the feeding period
and then the high-fat diet was replaced by standard diet
for the next 30 days of treatment period. Rats were
supplied food and water ad libitum.
Group I served as control received normal saline (5
ml/kg, per oral by oral feeding needle with tuberculin
syringe) daily for 30 days.
Group II served as hyperlipidemic diet and received
normal saline (5ml/kg, per oral by oral feeding needle
with tuberculin syringe) daily for 30 days.
Group III served as hyperlipidemic diet and received
Artemisia Judaica extract (50 mg/kg per oral by oral
feeding needle with tuberculin syringe) daily for 30
days.
Group IV served as hyperlipidemic diet and received
Panax ginseng extract (50 mg/kg per oral by oral
days.
Group V served as hyperlipidemic diet and received
Salvia officinalis extract (100 mg/kg per oral by oral
days.
Group VI served as hyperlipidemic diet and received
Polygonum multiflorum extract (400 mg/kg per oral by
oral feeding needle with tuberculin syringe) daily for 30
days.
Group VII served as hyperlipidemic diet and received
mixture of herbal extract (Artemisia Judaica + Panax
ginseng + Salvia officinalis + Polygonum multiflorum 50,
50, 100 and 400 mg/kg b.wt respectively, by oral
days.
Induction of hyperlipidemia
High fat diet (HFD) showed in Table 1
Table 1: Composition of experimental diets according to nutrition requirement center (NRC, 1998) [21].. by Feed soft enterprise
program 2010:
Formula Ingredients / kg BD HFD
Casein 5.0 5.0
Colic acid 2.0 2.0
Corn, Grain 57.8 32.8
Dical. Phos 0.1 0.1
DL-Methionine 0.1 0.1
L-Lysine HCl 0.1 0.1
Limestone 5.0 5.0
Methionine HA 0.1 0.1
Mineral Premix 0.1 0.1
Salt 1.0 1.0
Soybean Meal-44 23.7 28.7
Soybean Oil 5.0 25.0
Vitamin Premix 0.1 0.1

33
Composition chart
Animals were cared in accordance with standard
guidelines [22]. All blood samples were collected
within one hour period between 8:00am and 9:00
am. Twelve hours fasted blood samples were
collected under light ether anesthesia by retro
orbital puncture. Blood samples were collected
after 30 days of the treatment period. These blood
samples were used for serum lipid analysis and
inflammatory mediators. Then in the morning of
the 90th
day animal groups were sacrificed by
cervical dislocation after general anesthesia. Liver
was dissected out on ice quickly, cleaned and
stored at -80o
C till the preparation for analysis.
Liver homogenized in phosphate buffer slain 7.4 pH
using a homogenizer surrounded with an ice jacket
and the homogenates were used for the
determination of the oxidative stress marker
(MDA, GSH, GSSG, NO and 8-OH-dG) by HPLC.
Biochemical analysis Biochemical analyses of blood
and 10% of homogenate liver were assayed
according to the methods mentioned in table 1.
Statistical analysis
The values were expressed as the mean ± SE for
the 10 rats in each group. Differences between
groups were assessed by one way analysis of
variance (ANOVA) using SAS (2004) [23] software
for Windows (version 13.0). Statistical analysis of
the obtained data was performed using the general
linear model (GLM). Significant differences among
means were evaluated using Duncan’s (1955) [24].
Multiple Range Test.
The following linear model was applied:
Yij = μ + αi + ξij
Yij = Observation measured
Μ = Overallmean
αi = Effect of treatment .
ξij = Experimental error assumed to be randomly
distributed ( σ2 = 0 ).
Table 2: Methods and kits used to quantify the different biochemical analyses of blood and liver homogenate:
Parameters Method Company Reference
AST
Enzymatic-colorimetric Quimica Clinica Aplicada
S.A.(Amposta, Spain)
[25]
ALT
Enzymatic-colorimetric Quimica Clinica Aplicada
S.A.(Amposta, Spain)
[25]
Total Lipids (g/dl) Colorimetric Biodiagnostic ( Egypt) [26]
Cholesterol (mg/dl)
Colorimetric Stanbio Laboratory (Boerne,
Texas,78202 USA)
[27]
Triglycerides (g/dl) Colorimetric Stanbio Laboratory(Boerne, [28]

34
Texas,78202 USA)
HDL
Colorimetric Stanbio Laboratory (Boerne,
Texas,78202 USA)
[27]
LDL = TC-(TG/5)-HDL
MDA (nmol/g tissue) HPLC
Standard of 1, 1, 3, 3
tetraethoxypropane (Sigma)
[29]
GSH & GSSG HPLC
Standard of 1, 1, 3, 3
tetraethoxypropane (Sigma)
[30]
NO (nmol/g tissue) HPLC
Standard of nitite and nitrate
(Sigma).
[31]
8-OH-dG (nmol/g tissue) HPLC
Standard of 8 -hydroxy-2 –
deoxyguanosine (Sigma).
[32]
TNF-α ELISA RayBio ® Rat TNF- α USA [33]
IL-1β ELISA RayBio ® Rat IL-1 beta USA [33]
IL-6 ELISA RayBio ® Rat IL-6 USA [33]
Results
Table 3: Effect of AJ, PM, PG, SO and herbal mixture once daily for 28 days after 60 days HFD on serum ALT and AST of male albino
rats:
Groups
Parameters
ALT AST
Control 38.46 ± 1.32e
81.73 ± 2.82c
HFD 101.03 ± 1.72a
165.33 ± 2.8a
AJ 78.54 ± 3.12b
95.88 ± 3.81b
PG 80.08 ± 4.46b
95.20 ± 5.30b
SO 66.20 ± 3.21c
100.51 ± 4.88b
PM 65.21 ± 2.31c
101.49 ± 3.59b
AJ+PM++PG+SO 47.74 ± 2.17d
93.68 ± 4.26b
a, b, c, d, e means having different superscript letters in the same column differ significantly (P<0.05).
As shown in Table 3, serum ALT and AST levels were significantly increased (P<0.05) following administration
of HFD compared to the control group. However, treatment significantly showed enhancement in the
recorded liver function markers compared to HFD group.

35
Table 4: Effect of AJ, PM, PG, SO and herbal mixture once daily for 28 days after 60 days HFD on serum MDA, GSH, GSSG and NO of
male albino rats:
Groups
Parameters
MDA GSH GSSG NO 8-OH-dG
Control 11.82 ± 0.40d
15.76 ± 0.54a
0.612 ± 0.021e
0.309 ± 0.011f
298 ± 2.89d
HFD 28.75 ± 0.49a
11.02 ± 0.18d
3.24 ± 0.055a
2.054 ± 0.035a
423 ± 6.31a
AJ 18.63 ± 0.74b
12.56 ± 0.50cd
1.72 ± 0.068b
1.373 ± 0.055bc
372 ± 5.46b
PG 16.35 ± 0.91c
13.79 ± 0.76bc
1.53 ± 0.085c
1.474 ± 0.082b
379 ± 8.02b
SO 18.03 ± 0.87bc
15.13 ± 0.73ab
1.82 ± 0.088b
1.162 ± 0.056d
382 ± 8.27b
PM 12.08 ± 0.42d
15.038 ± 0.53ab
1.91 ± 0.068b
1.243 ± 0.044cd
370 ± 7.87b
AJ+PM++PG+SO 13.65 ± 0.62d
14.10 ± 0.64abc
0.806 ± 0.037d
0.677 ± 0.031e
358 ± 4.79c
a, b, c, d, e, f means having different superscript letters in the same column differ significantly (P<0.05).
As shown in Table 6, serum MDA, GSSG and NO levels were significantly increased and decrease in GSH level
(P<0.05) following administration of HFD compared to the control group. However, treatment significantly showed
enhancement in the recorded liver oxidative stress markers compared to HFD group.
Table 5: Effect of AJ, PM, PG, SO and herbal mixture once daily for 28 days after 60 days HFD on serum TL, T.Ch, TG, HDL and LDL of
male albino rats:
Groups
Parameters
TL TCh TG HDL LDL
Control 394 ± 13.6c
98 ± 3.3b
84 ± 2.9c
39 ± 1.3a
41 ± 1.4c
HFD 702 ± 11.9a
183 ± 3.1a
195 ± 3.3a
25 ± 0.4d
119 ± 2.0a
AJ 458 ± 18.2b
106 ± 4.2b
109 ± 4.3b
32 ± 1.2bc
52 ± 2.0b
PG 472 ± 26.3b
96 ± 5.39b
107 ± 5.9b
30 ± 1.6c
44 ± 2.5c
SO 483 ± 23.4b
99 ± 4.8b
108 ± 5.2b
34 ± 1.6b
42 ± 2.0c
PM 508 ± 18.0b
104 ± 3.7b
103 ± 3.6b
30 ± 1.0c
53 ± 1.8b
AJ+PM++PG+SO 401 ± 18.2c
103 ± 4.7b
101 ± 4.6b
35 ± 1.6ab
47 ± 2.1bc
a, b, c. means having different superscript letters in the same column differ significantly (P<0.05).
As shown in Table 4, serum TL, T.Ch, TG and LDL levels were significantly increased and decrease in HDL level
(P<0.05) following administration of HFD compared to the control group. However, treatment significantly showed
enhancement in the recorded of lipid profile markers compared to HFD group.
Table 6: Effect of AJ, PM, PG, SO and herbal mixture once daily for 28 days after 60 days HFD on serum TNFά, IL-1β and IL-6 of male
albino rats:
Groups
Parameters
TNFÜ IL-1â IL-6
Control 79.46 ± 2.74d
42.65 ± 1.47c
9.51 ± 0.32e
HFD 135.08 ± 2.30a
85.16 ± 1.45a
40.41 ± 0.68a
AJ 91.97 ± 3.65c
50.79 ± 2.02b
17.12 ± 0.68b
PG 89.59 ± 4.99cd
53.71 ± 2.99b
14.98 ± 0.83cd
SO 87.65 ± 4.25cd
55.60 ± 2.70b
15.90 ± 0.77bc
PM 102.78 ± 3.64b
54.71 ± 1.93b
13.49 ± 0.47d
AJ+PM++PG+SO 81.31 ± 3.70cd
42.54 ± 1.93c
10.51 ± 0.47e
a, b, c,d,e. means having different superscript letters in the same column differ significantly (P<0.05).

36
As shown in Table 5, serum TNFά, IL-1β and IL-6 levels were significantly increased (P<0.05) following administration of
HFD compared to the control group. However, treatment significantly showed regulation in the recorded of
inflammatory mediators compared to HFD group.
Discussion
Hyperlipidemia is one of the major modifiable risk
factors for stroke. The American Heart Association
states that treatment of hyperlipidemia reduces
risk of stroke by 30% [34]. Excessive quantities or
improper types of lipid-intake may result in
hyperlipidemia which is characterized by an
abnormal elevation in one or more of the serum
lipids such as total cholesterol (TC), low-density
lipoproteincholesterol (LDL-C) and triglycerides
(TG). The results showed that oxidative stress
induced by hyperlipidemic diet in rats was
characterized by retardation in body weight gain,
an increase in lipid peroxidation and elevation in
serum and liver biochemical markers of oxidative
stress. These findings were partially similar to
those obtained by Young et al. (1995) [35] who
reported that B.wt, lipid profile oxidative stress
marker and inflammatory mediators were greatly
increased, while HDL and GSH were significantly
decreased after 60 days high fat diet treated rats
when compared to the untreated control group.
The results are summarized in Table 3 and 4. As
shown, AJ decreased hepatic contents of ALT and
AST, MDA, GSSG, NO and 8-OH-dG and increased
their GSH contents as compared to HFD group. The
major bioactive compounds of defatted
alcoholic and water extracts of Artemisia
judaica essential oils (artemisyl-oil, apiperitone-oil,
piperitone and trans-ethyl cinnamate), saponins,
terpenes, tannins, and flavinoids (apigenin,
cirsimaritin, flavonoid glycosides) which have
antioxidant, anti-inflammation and anti-
hyperlipidemic activity [36]. Supplementation of
antioxidants may be a protective factor against
free radical induced cell damage [37]. Antioxidant
activity of AJ may be due to a significant level of
phenolic compounds including luteolin, luteolin-7-
glucoside, kaempferol, quercetin, rutin, coumarin
and so on [38]. The co-effectiveness of Artemisia
on hyperlipidemia and oxidative stress indicates a
strong point of this medicinal plant. Oxidative
stress is an early event in the evolution of
hyperlipidemia, and affects the development of
arteriosclerosis and myocardial infarction [39]. AJ
decreased lipid profile after 60 days of rats fed
HFD, indicating improvement of TL, TC, TG, LDL and
HDL. In agreement with the study of Jang et al.,
(2012) [40], they evaluated an antioxidant and
lipid-lowering effects of artemisia capillaris on a
Rat Model of Hyperlipidemia. Anti-hyperlipidemic
effect of AJ may be due to improve lipid
metabolism, body weight gain and adiposity and
that peroxisome proliferator-activated receptor-γ
(PPAR-γ) is associated with these events [41]. AJ
showed a significant decrease in TNF-α, IL-1β, and
IL-6 production. This further proves that AJ
regulates the inflammation by a significant
decrease of pro-inflammatory cytokines such as
TNF-α, IL-1β, and IL-6 by macrophages, which
mediates many crucial events for the initiation of
acute, sub acute and chronic inflammation. Also, it
is having an anti-proliferative activity and the
potential to directly react with free radicals [42].
Recently, Helal et al. (2015) [43] showed that
Artemisia judaica has a hepatoprotective effect
and improving liver function. This may be due to
the presence of flavonoids which have a
hypoglycemic action in addition to a potent
antioxidant action attenuating the oxidative stress
induced by free radicals, so they can ameliorate the
functions of the liver by protecting the hepatocytes
and inhibiting the production proinflammatory
mediators like TNF-α, IL-12, IL-2 cytokines which
has been associated with inflammatory diseases.
Results of the current study revealed that oral
administration of Panax ginseng (PG) to rats with
oxidative stress induce by HFD improved liver
function, reduced lipid peroxidation and decrease
inflammatory mediators. PG was found to possess
bioactive constituents which produce high
antioxidant activity and prevent oxidation of lipids.
Various phenolic compounds such as flavonoids,
phenolic acids, diterpenes, saponins and tannins
possess diverse biological activities and are thought
to be beneficial for reducing cell damage induced
by oxidative stress. The activity of phenolic
compounds might be related to their antioxidant
effect due to their ability to scavenge the free
radicals by presence of hydroxyl groups in these
compounds [44]. The hepatoprotective action of
PG reported in the present study was similar to
that obtained by [45]. Hypolipidemic effects of PG

37
were in accordance with those reported by Kawak
et al. (2010) and Shin et al. (2011) [46, 47]. The
antioxidant effect of PG, reported herein, agreed
with that previously reported by Lee et al. (2005)
[45]. Also, areduction in serum triglycerides level
was observed after treatment. These results were
in agreement with the results of [48]. who
mentioned that ginseng markedly reduced serum
triglycerides and cholesterol in hyperlipidemic
monkeys. In addition, Hwang et al. (2008) [49]
indicated that the administration of ginseng
saponins to rabbits fed high cholesterol diet
decreased the serum cholesterol level. In the
current study hypolipidemic effect of PG may be
due to saponins that, the natural appetite
suppressants. Ginsam increases PPAR- γ expression
and AMP-activated protein kinase phosphorylation
in liver and muscle. The extracts strongly activate
hormone specific lipase via protein kinase A.
Saponin reduce the absorption of cholesterol and
thus increase faecal excretion of cholesterol [50].
The inhibitory effect of PG on hyperlipidemia may
be due to inhibition of pancreaticlipase secretion
was mainly due to the characteristic structure of
saponin. Beyond lipase inhibition, other pathways
mediating the effect were also involved. Two
essential factors are noted here: one is the
suppression of the food intake with high
correlation to the body weight loss; the other is the
regulation of the cholesterol metabolism with the
resultant improvement of the lipoprotein
composition and the hepatic lipid-lowering effect
[51]. In the current study, it was found that PG
improved antioxidants' levels and decreased MDA,
GSSG, NO and 8-OH-dG levels in the treated group
when compared to the HFD group. In agreement,
Liu et al. (2003) [52] found that ginseng extracts
scavenge oxidative species; also, Surh et al. (2001)
[53] indicated that ginseng extracts attenuate lipid
peroxidation. That is, it may be related to saponins
which play a major role in antioxidant activities. In
addition, ginsenoides which are important
components heavily present in ginseng production
of powerful antioxidant activities other than radical
scavenging activities by stimulating gene
expression of antioxidant enzymes and enhancing
their activities [54]. In the present study, the mean
values of serum TNF-α, IL-1β and IL-6 were
increased in the HFD group and then improved by
ginseng treatment. These results were in
agreement with Kim et al. (2003) [55] who
reported that, ginseng saponins have been
proposed as possible candidates in the research of
therapeutic modulation of stress-related disorders,
for their inhibitory effect on the level of stress
induced IL-6 in mice. Moreover, Chun et al. (2007)
[56] indicated that ginsenoides inhibited the
lipopolysaccharide induced production of TNF-α by
blocking transcription factor (NF - KB) which
regulates the transcription of many gene
associated with inflammation.
Salvia officinalis (SO) showed hepato-protective
effect by decreasing activities of ALT and AST after
60 days HFD. Bassil et al. (2015) [57] revealed that
SO could significantly decrease the levels of ALT
and AST (P < 0.05) in serum of HFD rats. Treatment
with SO extract strongly decrease the level of
lipid peroxidation compared to HFD rats, which
may be due to its free radical scavenging
potential induced by HFD. It is known that SO
has inhibitory effect in lipid peroxidation
induced by Fe+2
and Cu+2
by its free radical
scavenging potential [58]. Because of central role
of transition metals in lipid peroxidation
process, our observations confirm the ability of
SO to scavenging free radicals and inhibition of
lipid peroxidation damage in HFD model. Ethanolic
extract of SO had a potent increasing effect on GSH
level decreasing MDA, GSSG, NO and 8-OH-dG on
liver tissues compared to HFD rats. Antioxidant
activity of SO may be due to phenolic and flavonoid
compounds are mainly responsible for the
antioxidant and free radical scavenging effect.
Antioxidant activity of SO was similar with
Nickavar, 2007; Yadav and Mukundan 2011 [59,
60]. Phenolic compounds such as carnosol, carnosic
and rosmarinic acids have a high antioxidative
activity and are usually extracted from SO with
ethanol [61]. The phenolic compounds can either
stimulate endogenous antioxidant defense systems
or scavenge reactive species [62]. The similar
results in another study confirmed that SO could
decrease the oxidative stress marker and increase
GSH in trichloroacetic acid induced increased
serum marker enzymes lipid peroxidation
antioxidative defense systems in rats [63].
Concerning the anti-obesity properties of SO, the
results presented here demonstrate that the lipid
profile of HFD rats treated with SO showed
neutralization of TC, TG, LDL and HDL. Anti-obesity
of SO may be due to pancreatic lipase inhibitor of

38
carnosic acid, Carnosic acid also significantly
inhibited triglyceride elevation in olive oil-loaded
mice and reduced the gain of body weight and the
accumulation of epididymal fat weight in high fat
diet-fed mice after 14 days [64]. Pancreatic lipase is
well known to play an important role in lipid
digestion [65]. The ethanolic extract from the
leaves of Salvia officinalis. Significantly inhibited
the pancreatic lipase activity, and suppressed
serum triglyceride (TG) elevation in olive oil-loaded
mice [64]. These results are compatible with
Christensen, (2010) [66] who concluded that SO
improved HDL and decreased lipid profile rat
serum fed HFD. Therapeutic effect of SO
significantly inhibited cytokine production (TNF-α,
IL-1β and IL-6) in serum rat fed HFD. Polygonum
multifurum (PM) (Polyphenolic compounds) have
an important role in stabilizing lipid oxidation and
are associated with antioxidant activity by lowering
ALT, AST, MDA, GSSG, NO and 8-OH-dG. These
results suggest that PM not only inhibits the
hepatic local inflammatory response, but also
attenuates the positive feedback loop between
oxidative stress and inflammation. The obtained
results confirmed with Abd El-Kader et al. (2012)
and Zhang, et al. (2012) [67,68] for antioxidant and
hepatoprotective activity of the plant who
suggested that polygonum stabilizing level of liver
function, oxidative stress markers and
inflammatory mediators. In present study, PM
group can significantly reduce the TL, TC, TG and
LDL in hyperlipidemic rats. This may be due to the
phenolic hydroxyls contained in phenolic
compounds, through oxidation. Cholesterol is
suppressed and unsaturated fatty acids are
oxidized. The obtained results confirmed with Xie,
et al. (2014) [69] for the lowering effect of
flavonoids (resveratrol) on lipid metabolism in
hyperlipidemic mice.
The present results also showed that the
antioxidant, anti-obesity and anti-inflammatory
effects of herbal cocktail was amplified by its co-
administration with AJ 50mg/kg B.wt, PG 50mg/kg
B.wt, SO 100 mg/kg B.wt and PM 400 mg/kg B.wt
after rats fed 60 days HFD.
Our study demonstrated that herbal cocktail
(mixture of AJ 50mg/kg B.wt, PG 50mg/kg B.wt, SO
100 mg/kg B.wt and PM 400 mg/kg B.wt) after rats
fed 60 days HFD could increase antioxidant
capacity, decrease oxidative stress markers,
decrease hyperlipidemia and inflammatory
mediators. Antihyperlipidemia of herbal cocktail
may be due to natural lipid metabolism regulators
of AJ, natural appetite suppressants of PG
(saponin), natural pancreatic lipase inhibitors of SO
(Carnosic acid) and suppresses the elevated mRNA
expression levels of sterol regulatory element-
binding protein-1c, peroxisome PPAR-γ, fatty acid
synthase, and adipocyte protein 2 in the white
adipose tissue of PM.
Acknowledgement
This research was supported by Sheikh Abdullah
bin Abdul Mohsen Al-Tuwaijri Stroke Chair (SATSC)
for Applied Research in stroke, Majmaah
University, Saudi Arabia. The authors would like to
express their gratitude towards Sheikh Abdullah
Abdul Mohsen Al-Tuwaijri, Rector Dr. Khalid Saad
Al Muqrin for providing the necessary support and
assistance in completing this piece of work.
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