Protective Effects of the Flavonoid-Rich Fraction from Rhizomes of Smilax glabra Roxb. on Carbon Tetrachloride-Induced Hepatotoxicity in Rats

Abstract

Hepatoprotective agents could prevent tissue damage and reduce morbidity and mortality rates; such agents may include folkloric or alternative treatments. The present study evaluated the protective effects of the flavonoid-rich fraction from rhizomes of Smilax glabra Roxb. (SGF) on carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. Sprague-Dawley male rats were orally treated with SGF daily and received CCl4 intraperitoneally twice a week for 4 weeks. Our results showed that SGF at doses of 100, 300 and 500 mg/kg significantly reduced the elevated activities of serum aminotransferases (ALT and AST), alkaline phosphatase and lactate dehydrogenase and the level of hepatic thiobarbituric acid-reactive substances compared to the CCl4-treated group. Moreover, SGF treatment was also found to significantly increase the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glutathione compared with CCl4-induced intoxicated liver. Histopathologic examination revealed that CCl4-induced hepatic damage was markedly reversed by SGF. The results suggest that SGF has hepatoprotective and antioxidant properties in CCl4-induced liver injury in rats.

Full text

Protective Effects of the Flavonoid-Rich Fraction from Rhizomes
of Smilax glabra Roxb. on Carbon Tetrachloride-Induced
Hepatotoxicity in Rats
Daozong Xia •Yongsheng Fan •Peihua Zhang •
Yan Fu •Mengting Ju •Xiaosa Zhang
Received: 21 February 2013 / Accepted: 6 May 2013 / Published online: 17 May 2013
Springer Science+Business Media New York 2013
Abstract Hepatoprotective agents could prevent tissue
damage and reduce morbidity and mortality rates; such
agents may include folkloric or alternative treatments. The
present study evaluated the protective effects of the fla-
vonoid-rich fraction from rhizomes of Smilax glabra Roxb.
(SGF) on carbon tetrachloride (CCl
4
)-induced hepatotox-
icity in rats. Sprague-Dawley male rats were orally treated
with SGF daily and received CCl
4
intraperitoneally twice a
week for 4 weeks. Our results showed that SGF at doses of
100, 300 and 500 mg/kg significantly reduced the elevated
activities of serum aminotransferases (ALT and AST),
alkaline phosphatase and lactate dehydrogenase and the
level of hepatic thiobarbituric acid–reactive substances
compared to the CCl
4
-treated group. Moreover, SGF
treatment was also found to significantly increase the
activities of superoxide dismutase, catalase, glutathione
peroxidase, glutathione reductase, glutathione-S-transfer-
ase and glutathione compared with CCl
4
-induced intoxi-
cated liver. Histopathologic examination revealed that
CCl
4
-induced hepatic damage was markedly reversed by
SGF. The results suggest that SGF has hepatoprotective
and antioxidant properties in CCl
4
-induced liver injury in
rats.
Keywords Smilax glabra Roxb. Flavonoids 
Membrane breakdown Hepatoprotection Carbon
tetrachloride Antioxidant
Introduction
Smilax glabra Roxb. (Liliaceae) is a traditional Chinese
herb, referred to as tufuling in Chinese medicine (Xia et al.
2010). The rhizome of S. glabra has been used in folk
medicine for the treatment of brucellosis (Chu and Ng
2006), syphilis (Galhena et al. 2012), acute and chronic
nephritis (Chen et al. 2000) and metal poisoning, such as
from lead, mercury and cadmium (Ng and Yu 2001; Xia
et al. 2010). In many Asian countries S. glabra is com-
monly used clinically to treat liver diseases, and a few
studies have indicated that it could inhibit human hepatoma
HepG2 and Hep3B cell growth (Thabrew et al. 2005;Sa
et al. 2008; Galhena et al. 2012). S. glabra extract (SGE)
could inhibit HepG2 and Hep3B cell growth by causing
cell-cycle arrest at either the S phase or the S/G
2
transition
and induce apoptosis, as evidenced by a DNA fragmenta-
tion assay (Sa et al. 2008). Moreover, the decoction com-
prised of S. glabra and two other herbs could significantly
inhibit the formation of paw edema in rats bearing early
hepatocarcinogenic changes (Galhena et al. 2012).
Some researchers have isolated and identified several
flavonoids (Chen et al. 1999), phenolics (Ng and Yu 2001)
and phenylpropanoid glycosides (Chen et al. 2000) from
rhizomes of S.glabra. Among these, smitilbin, engeletin,
D. Xia M. Ju X. Zhang
College of Pharmaceutical Sciences, Zhejiang Chinese Medical
University, No. 548, Binwen Road, Hangzhou 310053, Zhejiang
Province, China
Y. Fan (&)
President’s Office, Zhejiang Chinese Medical University, No.
548, Binwen Road, Hangzhou 310053, Zhejiang Province, China
e-mail: sigpx@sina.com; fyszjtcm@163.com
P. Zhang
Zhejiang Institute of Quality Inspection Science, No. 222,
Tianmushan Road, Hangzhou 310013, Zhejiang Province, China
Y. Fu
College of Biosystem Engineering and Food Science, Zhejiang
University, No. 866, Yuhangtang Road, Hangzhou 310058,
Zhejiang Province, China
123
J Membrane Biol (2013) 246:479–485
DOI 10.1007/s00232-013-9560-9

astilbin, eurryphin and resveratrol could protect against
hepatocyte damage from liver nonparenchymal cells
through selectively producing dysfunction of nonparen-
chymal cells with an essential requirement of rhamnose
(Chen et al. 1999; Ooi et al. 2004).
Carbon tetrachloride (CCl
4
) is a hepatotoxic agent that is
widely used to induce liver injury in experimental animals
in order to evaluate the antioxidant properties of possible
hepatoprotective agents (Pinto et al. 2012). During hepa-
totoxicity, cytochrome P450 metabolizes CCl
4
to trichlo-
romethyl radical (
•
CCl
3
) and trichloromethyl peroxy
radical (
•
OOCCl
3
) (Szymonik-Lesiuk et al. 2003). These
free radicals lead to the peroxidation of fatty acids found in
the phospholipids making up the cell membranes. Lipid
peroxide radicals, lipid hydroperoxides and lipid break-
down products develop in this process; and each constitutes
an active oxidizing agent (Cengiz et al. 2013). Conse-
quently, cell membrane structures and intracellular orga-
nelle membrane structures are completely broken down
and finally induce corresponding health problems (Preethi
and Kuttan 2009).
The general strategy for prevention and treatment of
liver damage includes reducing the production of reactive
metabolites and inhibiting the generation of free radicals
using antioxidants (Bansal et al. 2005). The methanol
extract of S. glabra rhizomes induced an increase of anti-
oxidant activities in V79-4 cell culture (Ooi et al 2004).
In a previous study (Xia et al. 2010), we reported that
SGE could significantly increase the glutathione (GSH)
content and alanine aminotransferase (ALT), superoxide
dismutase (SOD) and catalase (CAT) activities in lead-
exposed rats.
Although the inhibitory activity of S. glabra on hepa-
toma cell growth was investigated in vitro (Thabrew et al.
2005; Sa et al. 2008), scientific studies of S. glabra’s
usefulness with respect to liver injury induced by CCl
4
in
rats are lacking. Therefore, the present study evaluated the
protective effects of the flavonoid-rich fraction from rhi-
zomes of S. glabra Roxb. (SGF) on CCl
4
-induced hepa-
totoxicity in Sprague-Dawley male rats.
Materials and Methods
Plant Material and the Preparation of SGF
The rhizome of S. glabra was purchased from a local
vendor of Chinese medicinal herbs and identified by the
herbalist of Zhejiang Chinese Medical University. A vou-
cher sample was prepared and deposited at the herbarium
of Zhejiang Chinese Medical University. SGE was pre-
pared as described previously (Xia et al. 2010). Briefly, the
rhizome was air-dried, ground and extracted three times
with ethanol/water (60:40, v/v) at 80 C for 2 h each; then,
the extract was filtered through Whatman No. 1 filter paper,
and the ethanol from the extract was removed under vac-
uum. Then, the residue was dissolved in distilled water and
further fractionated with n-hexane, ethyl acetate and n-
butanol. Finally, the solvents from the fractionated extracts
were removed under vacuum and the residues lyophilized.
The dry powder of the ethyl acetate fraction as SGF was
chosen for the current study.
Total flavonoid content in SGF was measured as
described previously (Xia et al. 2011) and calculated as
rutin equivalents (milligrams per gram).
Animals
Sixty male Sprague-Dawley rats (190 ±10 g) were
obtained from SLAC Laboratory Animals (Shanghai,
China). Rats were acclimated to the experimental facility
for 1 week and housed in stainless steel cages in a room
with a 12 h dark/light cycle, an ambient temperature of
23 ±1C and relative humidity of 55 ±5 %. Rats were
allowed standard laboratory food and water (Xia et al.
2010). Our University Animal Care and Use Committee
approved the protocols for the animal study, and the ani-
mals were cared for in accordance with the ethical guide-
lines of Zhejiang University.
Experimental Design
Animals were randomly divided into six groups, with each
consisting of 10 rats. Group I received only vehicle, olive
oil (3 ml/kg) and 20 % DMSO (3 ml/kg). Animals of
groups II, III, IV and V received CCl
4
3 ml/kg (30 % in
olive oil, v/v) intraperitoneally (ip) twice a week for
4 weeks. Group II was treated with CCl
4
only, while
groups III, IV and V were treated with 3 ml/kg of SGF
dissolved in 20 % DMSO at dose levels of 100, 300 and
500 mg/kg by oral gavage, respectively, per day for
28 days. Animals of group VI were only given SGF
(500 mg/kg) daily by oral gavage. At the end of the
experimentation period, 24 h after the last treatment, all
animals were anesthetized with CO
2
, weighed and killed.
Blood samples were collected from all animals from the
retro-orbital venous plexus for biochemical variable anal-
ysis. Liver samples were dissected out, washed immedi-
ately with ice-cold saline to remove as much blood as
possible and immediately stored at -70 C until analysis.
An extra sample of liver was excised and fixed in 10 %
formalin solution for histopathologic analysis. Sections
(5 lm thick) were cut and stained with hematoxylin and
eosin for histological examination.
480 D. Xia et al.: S. glabra Rhizomes and Hepatotoxicity
123

Liver damage was assessed by estimation of serum
activities of ALT, aspartate aminotransferase (AST),
alkaline phosphatase (ALP) and lactate dehydrogenase
(LDH) using commercially available test kits from by
Nanjing Jiancheng Bioengineering Institute (Nanjing,
China). The results were expressed as units per liter.
The liver supernatant was used as a source to assay
enzymatic markers of oxidative stress, including SOD,
CAT, glutathione peroxidase (GPx), glutathione reductase
(GR) and glutathione-S-transferase (GST) activities. We
also determined GSH, thiobarbituric acid-reactive sub-
stances (TBARS) and the total protein content. GPx, GR
and GST were determined using commercially available
test kits from by Nanjing Jiancheng Bioengineering
Institute.
SOD, CAT, GSH and TBARS were determined
according to the methods described by us and others (Xia
et al. 2010; Ellman 1959; Marklund and Marklund 1974;
Saxena and Flora 2004), which are briefly reviewed below.
The level of GSH in hepatic supernatant was determined
according to the method of Ellman (1959). Supernatant
(0.02 ml) was added to 9 ml of distilled water. Then, 1 ml
of phosphate buffer (pH 8.0) was added. Subsequently,
0.02 ml 5,50-dithiobis(2-nitrobenzoic acid) was added to
3.0 ml of this solution. The results were expressed as the
contents (nanomoles of GSH) per milligram protein.
Hepatic tissue lipid peroxidation was measured by
shaking the 2 ml of liver homogenate (5 %, w/v) in
150 mM KCl, 0.025 M Tris–HCl buffer (pH 7.5) for
30 min at 37 C and measuring the malondialdehyde
formed with the thiobarbituric acid reaction. The amount of
TBARS was calculated using a molar extinction coefficient
of 1.56 910
5
M
-1
cm
-1
.
SOD activity in the hepatic supernatant was measured
using the method described by Marklund and Marklund
(1974). The reaction mixture was composed of supernatant
with 0.2 M pyrogallol, 1 mM EDTA and 50 mM Tris–HCl
(pH 8.2), in a final volume of 1 ml. The results were
expressed as units per minute per milligram of protein.
CAT activity in the hepatic supernatant was assayed
according to the method described by Aebi (1974). The
reaction mixture contained supernatant with 10 mM H
2
O
2
and 50 mM phosphate buffer (pH 7.0), in a final volume of
1 ml. The rate of decomposition of H
2
O
2
was measured.
Statistical Analysis
Data were expressed as mean ±standard error of the
mean. All statistical analyses were performed using SPSS
13.0 statistical software (SPSS, Inc., Chicago, IL). Signif-
icant differences among the treatment means were deter-
mined using analysis of variance and Duncan’s multiple
range tests. Results were considered statistically significant
at p\0.05.
Results
Total flavonoid content was estimated as 547 ±28.5 mg
rutin equivalents/g dry weight of SGF. Therefore, the high
content of flavonoids in SGF has strong antioxidant
potential to protect the damage in CCl
4
-treated rats.
The relative liver weights of each group of rats are
shown in Table 1. The results showed a significant increase
(p\0.05) of relative weight, by nearly 40 %, for CCl
4
-
treated rats compared to the normal control group. In
contrast, rats that received the indicated dose of SGF
showed a significant decrease (p\0.05) in liver weight
compared to the CCl
4
-treated group.
Results in Table 2revealed a significant elevation of
serum ALT, AST, ALP and LDH activities in CCl
4
-treated
group compared to normal controls (p\0.05), indicating
that CCl
4
induced significant damage to the hepatic cells.
Treatment of rats with SGF at 100, 300 and 500 mg/kg
markedly reduced (p\0.05) serum ALT, AST, ALP and
LDH activities in a dose-dependent manner compared to
the CCl
4
-treated group. These results suggested the
potential of SGF in protecting against liver injury on CCl
4
induction.
The histopathological changes induced by CCl
4
treatment
and by SGF are shown in Fig. 1. Compared with the liver
tissues of the normal controls, the liver tissue in the CCl
4
-
treated rats had extensive injuries, characterized by slight to
severe necrosis of hepatocytes, cell swelling, disruption of
membranes and contraction of the nucleus. Treatment with
SGF at 100, 300 and 500 mg/kg ameliorated the CCl
4
-
Table 1 Effect of the flavonoid-rich fraction from rhizomes of
Smilax glabra (SGF) on liver weights in CCl
4
-intoxicated rats
Groups Relative liver
weight (g/100 g)
Normal control 3.73 ±0.20
CCl
4
-treated 5.24 ±0.29
a,
**
SGF100 ?CCl
4
4.51 ±0.23
b,
*
SGF300 ?CCl
4
4.08 ±0.21
b,
**
SGF500 ?CCl
4
3.80 ±0.20
b,
**
SGF500 3.64 ±0.18
b,
**
SGF100 SGF 100 mg/kg, oral; SGF300 SGF 300 mg/kg, oral;
SGF500 SGF 500 mg/kg, oral
*p\0.05, ** p\0.01
a
Compared to the normal control group
b
Compared to the CCl
4
-treated group
D. Xia et al.: S. glabra Rhizomes and Hepatotoxicity 481
123

Table 2 Effect of the flavonoid-rich fraction from rhizomes of Smilax glabra (SGF) on serum activities of ALT, AST, ALP and LDH in CCl
4
-
intoxicated rats
Groups ALT (U/L) AST (U/L) ALP (U/L) LDH (U/L)
Normal control 32.1 ±1.74 96.4 ±4.75 103.2 ±5.01 491.7 ±26.43
CCl
4
-treated 73.1 ±4.12
a,
** 214.7 ±11.02
a,
** 242.7 ±11.64
a,
** 1,187.5 ±59.26
a,
**
SGF100 ?CCl
4
63.5 ±3.18
b,
* 186.9 ±9.48
b,
* 212.9 ±10.33
b,
* 992.7 ±51.42
b,
*
SGF300 ?CCl
4
47.3 ±2.33
b,
** 148.4 ±8.12
b,
** 168.5 ±8.72
b,
** 749.5 ±35.69
b,
**
SGF500 ?CCl
4
34.9 ±1.85
b,
** 115.9 ±5.81
b,
** 124.5 ±6.14
b,
** 553.0 ±27.64
b,
**
SGF500 31.2 ±1.62
b,
** 97.2 ±4.53
b,
** 102.9 ±5.03
b,
** 490.6 ±25.11
b,
**
SGF100 SGF 100 mg/kg, oral; SGF300 SGF 300 mg/kg, oral; SGF500 SGF 500 mg/kg, oral
*p\0.05, ** p\0.01
a
Compared to the normal control group
b
Compared to the CCl
4
-treated group
Fig. 1 Effects of the flavonoid-rich fraction from rhizomes of Smilax
glabra Roxb. (SGF) on liver histopathology stained with hematoxylin
and eosin. Normal control received only vehicles (olive oil and DMSO);
CCl
4
-treated received CCl
4
3 ml/kg (30 % in olive oil), ip; SGF100 ?
CCl
4
received SGF (100 mg/kg) ?CCl
4
, oral; SGF300 ?CCl
4
received SGF (300 mg/kg) ?CCl
4
, oral; SGF500 ?CCl
4
received
SGF (500 mg/kg) ?CCl
4
, oral; SGF500 received SGF (500 mg/kg),
oral. Scale bar =50 lm
482 D. Xia et al.: S. glabra Rhizomes and Hepatotoxicity
123

induced liver injury and markedly diminished the histolog-
ical alterations.
GSH and TBARS are widely used as markers of free
radical–mediated lipid peroxidation injury. Table 3shows
that CCl
4
treatment induced a significant decrease
(p\0.05) in the level of GSH in liver homogenates
compared to control livers. Treatment of rats with SGF at
100, 300 and 500 mg/kg significantly increased (p\0.05)
the hepatic GSH level in a dose-dependent manner com-
pared with the CCl
4
-treated group. Hepatic TBARS content
in the CCl
4
-treated group was significantly (p\0.05)
higher than that in the normal control group. In contrast,
rats that received the indicated dose of SGF showed a
significant increase (p\0.05) of the level of TBARS
compared to the CCl
4
-treated group.
Levels of SOD, CAT, GPx, GR and GST activities could
be regarded as an index of the antioxidant status of the
liver. The hepatic antioxidant enzymes SOD, CAT, GPx,
GR and GST, measured in rats with CCl
4
-induced liver
damage, respectively, showed 46, 38, 45, 45 and 54 % of
activity compared with the normal control group (Table 4).
There was a significant increase (p\0.05) in the activity
of these enzymes in the SGF-treated groups at different
doses compared to the CCl
4
-treated group.
The nontoxic effect of SGF was also supported by the
image in Fig. 1, which was in good correlation with the
results of the serum aminotransferases and hepatic anti-
oxidant enzyme activities.
Discussion
The liver is the main organ responsible for metabolism of
both endogenous and exogenous compounds; therefore, it
is also one of the first target organs for the toxic action of
xenobiotics or their reactive metabolites (Szachowicz-
Petelska et al. 2012). CCl
4
-induced hepatic injury is com-
monly used as an experimental method to study the hepa-
toprotective effects of natural products and drugs (Cengiz
et al. 2013). Oxidative stress and oxidative damage of cell
components caused by CCl
4
are counteracted by com-
pounds that have antioxidant properties. One of such potent
antioxidant is S.glabra, which is known as an herb to treat
various diseases in many Asian countries with a strong
in vitro antioxidant capacity (Sa et al. 2008); but its in vivo
antioxidant efficacy to CCl
4
-treated rats has not yet been
investigated.
This study was carried out to evaluate the protective
effects of SGF on CCl
4
-induced hepatotoxicity in rats.
Increases in serum AST, ALT, ALP and LDH levels have
been attributed to damaged structural integrity of the liver
because these enzymes are released into the circulation
after autolytic breakdown or cellular necrosis (Zhang et al.
2009). In the present study, we found that CCl
4
treatment
significantly increased the activities of serum AST, ALT,
ALP and LDH. Treatment with SGF in different doses
significantly inhibited CCl
4
-induced liver damage as evi-
denced by decreased serum aminotransferase, ALP and
LDH activities.
The increased formation of reactive oxygen species and
decreased antioxidant defense are defined as oxidative
stress, which is widely recognized as an important feature
of many diseases (Aydin et al. 2012). The antioxidant
defense systems exist to prevent the formation of these
increased reactive and free radicals. These include SOD-,
CAT- and GSH-related enzymes (GPx, GR and GST).
SOD is an exceedingly effective defense enzyme that
converts the dismutation of superoxide anions into
hydrogen peroxide (H
2
O
2
) (Reiter et al. 2000). CAT is
mainly a heme-containing enzyme. The predominant
subcellular localization of enzyme is in the peroxisomes,
in which it catalyzes the dismutation of hydrogen peroxide
to water and molecular oxygen (Aydin et al. 2012). GPx
plays an important role in the detoxification of xenobiotics
in the liver and catalyzes the reduction of H
2
O
2
and
hydroperoxides to nontoxic products (Hsu et al. 2008). GR
is a cytosolic hepatic enzyme involved in the detoxifica-
tion of a range of xenobiotic compounds by their conju-
gation with GSH (Naik and Panda 2007). GSTs catalyze
the conjugation of GSH to a variety of compounds con-
taining an electrophilic center and have been found in all
tissues and organisms examined to date (Leaver and
George 1998). In our study, the activity of antioxidant
enzymes, such as SOD, CAT, GPx, GR and GST, sig-
nificantly decreased in liver tissue of CCl
4
-treated rats.
However, administration of SGF significantly decreased
the toxicity of CCl
4
and increased the activities of these
antioxidant enzymes.
Table 3 Effect of the flavonoid-rich fraction from rhizomes of
Smilax glabra (SGF) on hepatic GSH and TBARS concentrations in
CCl
4
-intoxicated rats
Groups GSH
(nmol/mg protein)
TBARS
(nmol/g tissue)
Normal control 19.8 ±1.45 168.4 ±12.75
CCl
4
-treated 9.1 ±0.67
a,
** 317.6 ±20.25
a,
**
SGF100 ?CCl
4
12.2 ±0.91
b,
** 275.6 ±18.48
b,
*
SGF300 ?CCl
4
16.4 ±1.22
b,
** 222.9 ±15.15
b,
**
SGF500 ?CCl
4
19.3 ±1.48
b,
** 186.3 ±11.98
b,
**
SGF500 20.2 ±1.51
b,
** 167.6 ±9.58
b,
**
SGF100 SGF 100 mg/kg, oral; SGF300 SGF 300 mg/kg, oral;
SGF500 SGF 500 mg/kg, oral
*p\0.05, ** p\0.01
a
Compared to the normal control group
b
Compared to the CCl
4
-treated group
D. Xia et al.: S. glabra Rhizomes and Hepatotoxicity 483
123

In addition, treatment with SGF significantly elevated
the GSH content in the liver of rats, suggesting that SGF
could protect against the CCl
4
-induced depletion of hepatic
GSH. Moreover, the significant increase in the hepatic GR
activity and GSH content confirm that treatment with SGF
could effectively protect against the hepatic oxidative
damage by GSH regenerated from glutathione disulfide
(Pinto et al. 2012).
TBARS are major reactive aldehydes resulting from the
peroxidation of polyunsaturated fatty acids. They are useful
indicators of tissue damage, including a series of chain
reactions (Khan et al. 2012). S. glabra is rich in flavonoids
and phenolic compounds, providing protection from lipid
peroxidation. Flavonoids and phenolics have high antiox-
idant capacity and have been shown to be effective anti-
oxidants in inhibiting lipid peroxidation as well as potent
radical scavengers (Xia et al. 2010). In this study, CCl
4
-
induced toxicity caused an increase of TBARS levels in the
liver tissue compared to the normal control group. Treat-
ment with SGF could reverse these changes and caused a
significant decrease in TBARS levels compared to the
CCl
4
-induced hepatic toxicity in rats.
Histopathologic analysis in this study revealed that
CCl
4
-induced hepatic damage was markedly reversed by
SGF. These data are in good agreement with the results for
the activities of the serum aminotransferases ALP and
LDH as well as that of hepatic antioxidant enzymes.
In conclusion, our results provide evidence for the
effectiveness of SGF in prevention of CCl
4
-induced oxi-
dative stress and hepatic damage. This indicates the pos-
sibility of the use of this natural antioxidant in preventing
disorders initiated by oxidative stress. Furthermore, SGF
may be useful as a hepatoprotective agent against chemi-
cal-induced hepatotoxicity in vivo.
Acknowledgments This work was supported by the National Nat-
ural Science Foundation of China (Grant 81102861), the Zhejiang
Provincial Natural Science Foundation of China (Grant Y2110031)
and the China Postdoctoral Science Foundation (Grants 2012T50562,
20110491827).
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Table 4 Effect of the flavonoid-rich fraction from rhizomes of Smilax glabra (SGF) on hepatic antioxidant enzymes activity in CCl
4
-intoxicated
rats
Groups SOD
(U/min/mg protein)
CAT (lmol H
2
O
2
consumed/min/mg protein)
GPx (U/mg protein) GST (U/mg protein) GR (U/g protein)
Normal control 19.8 ±1.44 57.2 ±3.63 120.1 ±7.44 18.1 ±1.28 3.79 ±0.28
CCl
4
-treated 10.6 ±0.77
a,
** 35.4 ±2.09
a,
** 65.2 ±4.13
a,
** 9.8 ±0.73
a,
** 1.71 ±0.12
a,
**
SGF100 ?CCl
4
13.9 ±1.10
b,
** 40.5 ±2.42
b,
* 77.5 ±6.21
b,
** 10.7 ±0.64 2.50 ±0.15
b,
**
SGF300 ?CCl
4
15.8 ±1.25
b,
** 45.3 ±2.98
b,
** 100.1 ±7.07
b,
** 14.2 ±1.06
b,
** 3.21 ±0.22
b,
**
SGF500 ?CCl
4
18.0 ±1.31
b,
** 50.2 ±3.24
b,
** 111.6 ±7.13
b,
** 16.2 ±1.21
b,
** 3.53 ±0.24
b,
**
SGF500 19.6 ±1.45
b,
** 57.5 ±3.68
b,
** 121.5 ±7.68
b,
** 18.0 ±1.26
b,
** 3.81 ±0.29
b,
**
SGF100 SGF 100 mg/kg, oral; SGF300 SGF 300 mg/kg, oral; SGF500 SGF 500 mg/kg, oral
*p\0.05, ** p\0.01
a
Compared to the normal control group
b
Compared to the CCl
4
-treated group
484 D. Xia et al.: S. glabra Rhizomes and Hepatotoxicity
123

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