Preventive and curative effects of Artemisia absinthium on acetaminophen and CCl4-induced hepatotoxicity

• 1.1. Effect of aqueous-methanolic extract of Artemisia absinthium (Compositae) was investigated against acetaminophen- and CCl₄-induced hepatic damage.
• 2.2. Acetaminophen produced 100% mortality at the dose of 1 g/kg in mice while pretreatment of animals with plant extract (500 mg/kg) reduced the death rate to 20%.
• 3.3. Pretreatment of rats with plant extract (500 mg/kg, orally twice daily for two days) prevented (P < 0.01) the acetaminophen (640 mg/kg) as well as CCl₄ (1.5 ml/kg)-induced rise in serum transaminases (GOT and GPT).
• 4.4. Post-treatment with three successive doses of extract (500 mg/kg, 6 hr) restricted the hepatic damage induced by acetaminophen (P < 0.01) but CCl₄-induced hepatotoxicity was not altered (P > 0.05).
• 5.5. Plant extract (500 mg/kg) caused significant prolongation (P < 0.05) in pentobarbital (75 mg/kg)-induced sleep as well as increased strychnine-induced lethality in mice suggestive of inhibitory effect on microsomal drug metabolizing enzymes (MDME).
• 6.6. These results indicate that the crude extract of Artemisia absinthium exhibits hepatoprotective action partly through MDME inhibitory action and validates the traditional use of plant in hepatic damage.

     

The effect of chondroitin sulfate against CCl4-induced hepatotoxicity

This study was conducted to develop a new biomaterial to be used for an antioxidative drug. In this study, the hepatoprotective effect of chondroitin sulfate (CS) (100 mg/kg and 200 mg/kg body weight) was investigated at the antioxidative enzyme levels of liver total homogenate and mitochondria fraction. And the carbone tetrachloride (CCl(4))-induced rats were used as hepatotoxic models. The CCl(4) induced rat has been widely used as a hepatotoxic model due to its practicality, convenience and cost effectiveness since the generation of free oxygen radicals by CCl(4) injection was proposed as an important causative agent of hepatotoxicity. Malondialdehyde (MDA) levels were determined as well as the activities of superoxide dismutase (SOD), catalase (CAT), reduced-glutathione (GSH), oxidized-glutathione (GSSG) and glutathione peroxidase (GPx) in the liver. In addition, histopathology of liver tissue was investigated. Liver antioxidative enzyme activity was elevated while MDA concentration was decreased in all CS treated animals. The results demonstrated that CS protected oxidative stress in a dose dependent manner. Moreover, inflammation and cirrhosis in liver tissue of CS treated group were significantly decreased. It gave us an impression that CS might be a radical scavenger.     

Hepatoprotective effect of ethanol extract from Berchemia lineate against CCl4-induced acute hepatotoxicity in mice

Abstract

Context: The roots of Berchemia lineate (L.) DC. (Rhamnaceae) have been long used as a remedy for the treatment of some diseases in Guangxi Province, China.

Objective: The present study investigates the hepatoprotective effect of Berchemia lineate ethanol extract (BELE) on CCl₄-induced acute liver damage in mice.

Materials and methods: Effect of BELE administrated for 7 consecutive days was evaluated in mice by the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin (TBIL), albulin (ALB), globulin (GLB), and total protein (TP) levels, as well as liver superoxide dismutase (SOD) activity and malondialdehyde (MDA) level. Moreover, histopathological examinations were also taken.

Results: Compared with the model group, administration of 400?mg/kg BELE for 7?d in mice significantly decreased the serum ALT (56.25?U/L), AST (297.67?U/L), ALP (188.20?U/L), and TBIL (17.90?mol/L), along with the elevation of TP (64.67?g/L). In addition, BELE (100, 200, and 400?mg/kg, i.g.) treated mice recorded a dose-dependent increment of SOD (291.17, 310.32, and 325.67?U/mg prot) and reduction of MDA (7.27, 6.77, and 5.33?nmol/mg prot) levels. Histopathological examinations also confirmed that BELE can ameliorate CCl₄-induced liver injuries, characterized by extensive hepatocellular degeneration/necrosis, inflammatory cell infiltration, congestion, and sinusoidal dilatation.

Discussion and conclusion: The results indicated that BELE possessed remarkable protective effect against acute hepatotoxicity and oxidative injuries induced by CCl₄, and that the hepatoprotective effects of BELE may be due to both the inhibition of lipid peroxidation and the increase of antioxidant activity.     

Inhibitory effect of Nymphaea pubescens Willd. flower extract on carrageenan-induced inflammation and CCl4-induced hepatotoxicity in rats

Nymphaea pubescens Willd. is used as ingredient of ethnic diet and folk medicine in South-East Asia. The water (NPW), methanol (NPM) and chloroform (NPC) extracts of N. pubescens flowers were investigated for NO, ${\text{O}}_2^{\text{<mglyph src="https://sdfestaticassets-us-east-1.sciencedirectassets.com/shared-assets/16/entities/rad"></mglyph>}-}$ and DPPH radical scavenging and iron chelating activities in vitro. NPW was found to be the most potent free radical scavenger (EC₅₀ < 100 μg/mL) whereas NPC did not show EC₅₀ at 500 μg/mL. Therefore, NPW was selected for further studies on anti-inflammatory and hepatoprotective activities, using standard in vitro and in vivo models. NPW exhibited inhibition of nitrogen radical generation in LPS-activated macrophages (IC₅₀ = 75.5 μg/mL) through suppression of iNOS protein, with no associated toxicity in the cells. Further, 500 mg/kg of NPW reduced rat paw edema by ∼50% after 6 h of carrageenan administration. Hepatoprotective activity of NPW was also evaluated in vivo on CCl4-induced hepatotoxicity model in rats. NPW treatment (500 mg/kg/day for ten days) attenuated CCl4-induced increase in serum enzymes, viz. alanine and aspartate aminotransferases (ALT and AST) and bilirubin. Also, glutathione and superoxide dismutase (SOD)-levels were restored towards normalcy in the liver of CCl4-treated rats, indicating the hepatoprotective role of NPW, which was found to contain a fair amount of flavonoids, phenolics, and saponin constituents.     

Protective effect of S-adenosyl-L-methionine against CCl4-induced hepatotoxicity in cultured hepatocytes

Effect of S-adenosyl-L-methionine disulfate tosylate salt (SAMe-ST) and L-methionine (L-Met) on primary cultured rat hepatocytes were studied. In cultured hepatocytes treated with CCl4, SAMe-ST and L-Met suppressed the decrease in urea-nitrogen secretion as well as the leakages of GOT and GPT. The membrane-protective action of these two compounds was verified by the histological data. Failure of SAMe-ST to counteract CCl4-induced reduction of radioactive leucine incorporation into the trichloroacetic acid-insoluble materials in hepatocytes indicates that the observed effects of SAMe-ST or L-Met do not involve acceleration of protein synthesis. The present results indicate that SAMe-ST remarkably protects hepatocytes from CCl4-induced hepatotoxicity, probably by either changing the structure or compositions of membrane phospholipids or by modifying the interaction of CCl4 with the intracellular drug-metabolizing enzyme systems.     

Hepatoprotective activity of methanolic extract of Hiptage bengalensis leaves against CCl4-induced hepatotoxicity in rats

The objective of the present study was to evaluate hepatoprotective activity of methanolic extract of Hiptage bengalensis (L.) kurz (MEHB) in rats. Hepatic damage was induced by administration of carbontetrachloride(1 ml/kg, b.w, p.o.) in combination with liquid paraffin (1:1) as a single dose on 7th day. The extent of liver damage was studied by estimating biochemical parameters. Administration of MEHB (200 mg & 400 mg/kg) for 6 days before carbontetrachloride administration showed a significant reduction (p < 0.01) of serum liver damage enzymes markers-aspartate transaminase, alanine transaminase, total bilirubin and alkaline phosphatase (ALP). Histopathological changes of hepatic tissue were also evaluated in control and MEHB treated groups. Results also indicated that MEHB possessed potential antioxidant effect by increasing the levels of glutathione and also possessed free radical scavenging activities. The hepatoprotective effect of Hiptage bengalensis (L.) kurz was comparable to standard drug silymarin (50 mg/kg).     

The protective effects of Hibiscus sabdariffa extract on CCl4-induced liver fibrosis in rats.

Dried flower Hibiscus sabdariffa L. (HSE) extracts, a local soft drink material and medicinal herb, were studied for their protective effects against liver fibrosis induced using carbon tetrachloride (CCl(4)) in rats. Male Wistar rats were administered CCl(4) by intraperitoneal injection for 7weeks and received a normal diet or normal diet with various HSE doses (1-5%) for 9weeks. HSE significantly reduced the liver damage including steatosis and fibrosis in a dose dependent manner. Moreover, HSE significantly decreased the elevation in plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT). It also restored the decrease in glutathione content and inhibited the formation of lipid peroxidative products during CCl(4) treatment. In the primary culture, HSE also significantly inhibited the activation of the hepatic stellate cells. These results suggested that HSE may protect the liver against CCl(4)-induced fibrosis. This protective effect appears due to HSEs antioxidant properties.     

Hepatoprotective and antioxidant effects of baicalin against CCl4-induced hepatotoxicity

Scutellaria baicalensis is widely cultivated in eastern Asia, particularly in China. In the present study, we isolated baicalin from this plant and studied for its hepatoprotective activity against CCl₄-induced oxidative damage in rats. Our findings revealed that baicalin exhibited strong antioxidant activity in vitro. In established in vivo tests, baicalin showed effective protective effects by reducing the elevated levels of glutamate pyruvate transaminase(ALT), aspartate aminotransferase(AST), alkaline phosphatase (ALP), total bilirubin (TB) and malondialdehyde (MDA) against CCl₄-induced damage, and it restored the activities antioxidant defense substances, such as superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH), toward their normal levels. These data were supplemented with histopathological examination of rat liver sections. The results demonstrated that baicalin could be proposed to protect the liver against CCl₄-induced oxidative damage in rats, and the possible underlying mechanism of the activity could be due to its free radical-scavenging and antioxidant activity.     

Chemical composition and protective effect of Juniperus sabina L. essential oil against CCl4 induced hepatotoxicity

The hepatoprotective activity of the total extract of Juniperus sabina L. against CCl₄ induced toxicity in experimental animals was previously reported and indicated promising results. Essential oil of J. Sabina was prepared by hydrodistillation method. Components of the oil were identified by comparison of GC-MS and retention indexes with reported data. The hepatoprotective effect of the essential oil against CCl₄ induced toxicity was studied using male Wistar rats and silymarin at 10 mg/kg p.o as standard drug. The protective effect was evaluated via serum biochemical parameters such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyltranspeptidase (GGT), and total bilirubin as well as tissue parameters including non-protein sulfhydryl groups (NP-SH), malonaldehyde (MDA) and total protein (TP). Histopathological study was applied on the liver tissues using Mayer’s hematoxylin stain, Periodic Acid Schiff – Hematoxylin (PAS-H) and Masson trichrome technique on light microscope. Electron microscope images were also obtained for more detailed study.     

Differential acute effects of phenobarbital and 3-methylcholanthrene pretreatment on CCl 4 -induced hepatotoxicity in rats

Phenobarbital (PB) pretreatment significantly enhanced the rise in SGOT and SGPT activity immediately after a 3 hr exposure of rats to CCl₄ by inhalation. However, these parameters of hepatotoxicity were significantly lower in rats pretreated with 3-methylcholanthrene (MC) when compared to rats pretreated with the vehicle and exposed to CCl₄ vapor. Hepatic microsomal NADPH cytochrome c reductase activity and the amount of CO-binding pigment were elevated by PB pretreatment, but MC had no effect on hepatic microsomal NADPH cytochrome c reductase activity. Although CCl₄ exposure reduced CO-binding pigment content by 61% in PB pretreated and by 39% in MC-pretreated rats, microsomal NADPH cytochrome c reductase activity was reduced by only 6% and 20%, respectively. At 21 hr after exposure to CCl₄, the difference in SGOT and SGPT values of the PB and MC pretreated rats was more divergent. Histologic evidence at this time revealed extensive damage in the PB pretreated animals and a sparing effect in the MC pretreated animals. The differential effects of MC and PB pretreatment on NADPH cytochrome c reductase activity and CO-binding pigment content may be responsible for the observed protective effect of MC in CCl₄ exposed rats.     

Hepatoprotective effect of cold-pressed Syzygium aromaticum oil against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats

Contexts: Exposure to environmental pollutants such as carbon tetrachloride (CCl₄) causes liver injuries. There are claims that extracts from Syzygium aromaticum (Linn.) Merrill & L.M.Perry, (Myrtaceae) protects from such injuries.

Objective: This study investigates the protective effects of cold-pressed S. aromaticum oil (CO) against CCl₄-induced liver toxicity in rats.

Materials and methods: CO was orally administered to rats in two doses (100 and 200?mg/kg) along with CCl₄ (1 mL/kg in olive oil) for 8 weeks. Indices of liver and kidney functions, lipid profile, and peroxidation were evaluated in rats’ serum and tissues. Fatty acids and bioactive lipids of CO were analyzed.

Results: High levels of monounsaturated fatty acids (39.7%) and polyunsaturated fatty acids (42.1%) were detected in CO. The oil contained high amounts of tocols and phenolics. The LD₅₀ value at 24 h was approximately 5950?mg/kg. Treatment with 200?mg/kg CO resulted in a decrease of creatinine, urea, and uric acid levels to 0.86, 32.6, and 2.99?mg/dL, respectively. Levels of TL, TC, TAG, LDL-C, and VLDL-C were decreased to 167, 195.3, 584.5, 74.6, and 39.0?mg/L, respectively, after 8 weeks of treatment. Hepatic malondialdehyde levels were reduced and glutathione levels were elevated in CO-treated rats. CO reduced the activities of AST, ALT, and ALP as well as kidney function markers, protein, and lipid profiles, respectively. Histopathological examination of liver indicated that CO treatment reduced fatty degenerations, cytoplasmic vacuolization, and necrosis.

Conclusion: CO possessed a protective effect against CCl₄-induced hepatotoxicity in rats, mediated possibly by the antioxidant properties of the oil.     

Selective protective effect of an extract from Fumaria parviflora on paracetamol-induced hepatotoxicity

• 1.1. The hepatoprotective activity of an aqueous-methanolic extract of Fumaria parviflora was investigated against paracetamol- and CCl₄-induced hepatic damage.
• 2.2. Paracetamol (1 g/kg; orally) produced 100% mortality in mice; pretreatment of animals with the plant extract (500 mg/kg; orally) reduced the death rate to 50%.
• 3.3. Pretreatment of rats with plant extract (500 mg/kg, orally twice daily for 2 days) prevented (P<0.001) the paracetamol (640 mg/kg)-induced rise in serum enzymes alkaline phosphatase (ALP) and transaminases (GOT and GPT), whereas the same dose of the extract was unable to prevent (P>0.05) the CCl₄-induced rise in serum enzyme levels.
• 4.4. Posttreatment with 3 successive doses of the extract (500 mg/kg, 6 hourly) also restricted the paracetamol-induced hepatic damage.
• 5.5. The plant extract (500 mg/kg; orally) caused significant prolongation in pentobarbital (75 mg/ kg)-induced sleep as well as increased strychnine-induced lethality in mice (P<0.05), suggestive of an inhibitory effect on microsomal drug metabolizing enzymes (MDME).
• 6.6. It is conceivable therefore, that Fumaria parviflora extract exhibits a selective protective effect against paracetamol-induced hepatotoxicity, probably mediated through MDME inhibition.

     

Studies on protective effect of DA-9601,Artemisia asiatica extract, on acetaminophen- and CCI4-induced liver damage in rats

The hepatoprotective effect of DA-9601, a quality-controlled extract ofArtemisia asiatica, on liver damage induced by acetaminophen (APAP) and carbon tetrachloride (CCI₄) was investigated by means of serum-biochemical, hepatic-biochemical, and histopathological examinations. Doses of DA-9601 (10, 30, or 100mg/kg) were administered intragastrically to each rat on three consecutive days i.e. 48 h, 24 h and 2 h before a single administration of APAP (640 mg/kg, i.p.) or CCl₄ (2 ml/kg, p.o.). Four h and 24 h after hepatotoxin treatment, the animals were sacrificed for evaluation of liver damage. Pretreatment of DA-9601 reduced the elevation of serum ALT, AST, LDH and histopathological changes such as centrilobular necrosis, vacuolar degeneration and inflammatory cell infiltration dose-dependently. DA-9601 also prevented APAP- and CCl₄-induced hepatic glutathione (GSH) depletion and CCl₄-induced increase of hepatic malondialdehyde (MDA), a parameter of lipid peroxidation, in a dose-dependent manner. These findings suggest that pretreatment with DA-9601 may reduce chemically induced liver injury by complex mechanisms which involve prevention of lipid peroxidation and preservation of hepatic GSH.     

Potentiation of CCl4-induced hepatotoxicity in the dog by chronic exposure to phenobarbital

Carbon tetrachloride (CCl₄) hepatotoxicity was studied in normal and in phenobarbital-pretreated beagle dogs. The liver content of triglycerides (TG) and lipid peroxides, and activities of microsomal enzymes as well as serum glutamicoxaloacetic (SGOT) and glutamic-pyruvic (SGPT) transaminases were monitored for periods up to 24 hr after CCl₄ administration. CCl₄ alone produced no consistent changes in the parameters studied. Phenobarbital pretreatment produced significant increases in liver TG content, microsomal enzyme activities and SGPT activity. Phenobarbital pretreatment had no effect on CCl₄-induced changes in glucose-6-phosphatase activity, but produced an immediate increase in lipid peroxide content, which declined to normal by 24 hr after treatment. The TG content of livers from phenobarbital-pretreated dogs began to increase by 3 hr after CCl₄ administration and continued to increase as the time after administration increased. Activities of SGOT and SGPT were strikingly increased 3 hr after administration of CCl₄ and were still apparently increasing 24 hr after treatment. CCl₄ administration to phenobarbital-treated dogs eliminated the increase in activities of all microsomal drug-metabolizing enzymes that were seen with phenobarbital pretreatment alone. It was concluded that phenobarbital produced a true potentiation of the toxicity of CCl₄ by apparently decreasing the threshold at which the hydrocarbon becomes toxic. The results produced no definitive evidence to explain the mechanism by which phenobarbital produces the increase in CCl₄ toxicity.     

Ameliorative effects of 7-methylcoumarin and 7-methoxycoumarin against CCl4-induced hepatotoxicity in rats

The available conventional remedies for the treatment of drug-induced liver diseases are highly inadequate and possess serious adverse effects; therefore, the development of new, effective drugs is considered necessary. This article explores the hepatoprotective and antioxidant potential of 7-methylcoumarin (MC) and 7-methoxycoumarin (MOC) in CCl₄-induced hepatotoxicity in rats. MC and MOC individually, at doses of 50 and 100 mg/kg body weight, were administered orally once-daily for 7 days. The hepatoprotective activity was assessed using various biochemical parameters, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), serum bilirubin (TB), total protein (TP), and albumin (TA). Serum antioxidant enzyme [e.g., superoxide dismutase (SOD) and catalase (CAT)] levels were determined. Also, thiobarbituric-acid–related substances (TBARS) levels, along with histopathological studies of liver tissue, were scrutinized. Pretreatment with MC and MOC significantly decreased ALT, AST, and TB in the serum of CCl₄-induced liver damaged rats in a dose-dependent manner. TA and TP levels in the serum were also restored significantly in all presupplemented MC and MOC groups. In addition, oxidative stress induced by CCl₄ was prevented significantly; thereby, increasing SOD and CAT levels and decreasing TBARS levels in liver homogenates. Histopathological studies revealed the ameliorative natures of both the compounds. This study demonstrates the strong hepatoprotective activity of MC and MOC, which could be attributed to their potent antioxidant effects.     

Ameliorative effect of methanol extract of Rumex vesicarius on CCl4-induced liver damage in Wistar albino rats

Abstract

Context: Rumex vesicarius L. (Polygonaceae), an edible plant, is reported to have many bioactive phytochemicals, especially flavonoids and anthraquinones with antioxidant and detoxifying properties.

Objective: This study evaluated the methanolic extract of R. vasicarius (MERV) for hepatoprotective activity in rats against CCl₄-induced liver damage.

Materials and methods: The whole plant extract was prepared and investigated for its hepatoprotective activity. Rats were pretreated with MERV (100 and 200?mg/kg, p.o.) for 7?d prior to the induction of liver damage by CCl₄. Animals were then sacrificed 24?h after CCl₄ administration for the biochemical (AST, ALT, and ALP activity in serum; lipid peroxidation (LPO) and glutathione (GSH) levels in liver tissue) and histological analyses.

Results: CCl₄-induced hepatotoxicity was confirmed by an increase (p?<?0.05) in serum AST (4.55-fold), ALT (3.51-fold), and ALP (1.82-fold) activities. CCl₄-induced hepatotoxicity was also manifested by an increase (p?<?0.05) in LPO (3.88-fold) and depletion of reduced glutathione (3.14-fold) activity in liver tissue. The multiple dose MERV administration at 200?mg/kg showed promising hepatoprotective activity as evident from significant decrease levels of serum AST (230.01?±?13.21), serum ALT (82.15?±?5.01), serum ALP (504.75?±?19.72), hepatic LPO (3.38?±?0.33), and increased levels of hepatic glutathione (0.34?±?0.04) towards near normal. Further, biochemical results were confirmed by histopathological changes as compared with CCl₄-intoxicated rats.

Discussion and conclusion: The results obtained from this study indicate hepatoprotective activity of Rumex plant against CCl₄-induced liver toxicity; hence, it can be used as a hepatoprotective agent.     

Studies on the protective effect of flaxseed oil on cisplatin-induced hepatotoxicity

Cisplatin (CP) is known as one of the most potent chemotherapeutic antitumor drugs. The tissue-specific toxicity of CP in the kidneys is well documented. However, at higher doses less common toxic effects such as hepatotoxicity may arise. Since CP remains one of the most effective antineoplastic drug used in chemotherapy, strategies to protect tissues against CP toxicity are of clinical interest. Recently, ω-3 polyunsaturated fatty acids (PUFAs) from certain plants/seeds notably flaxseed have shown numerous health benefits. In view of this, the present study investigates the protective effect of flaxseed oil (FXO) on CP-induced damage in liver. Rats were pre-fed normal diet and the diet rich in FXO for 10 days and then a single dose of CP (6 mg/kg body weight) was administered intraperitoneally while still on diet. Serum/urine parameters, enzymes of carbohydrate metabolism and oxidative stress were analyzed. CP caused perturbation of the antioxidant defense as reflected by the decrease in the activities of catalase, superoxide dismutase and glutathione peroxidase. Further the activities of various enzymes involved in glycolysis, tricarboxylic acid cycle, gluconeogenesis and hexose monophosphate shunt pathways were determined and were found to be differentially altered by CP treatment. However, these alterations were ameliorated in CP-treated rats fed on FXO. Present results show that dietary supplementation of FXO in CP-treated rats ameliorated CP-induced hepatotoxic and other deleterious effects due to its intrinsic biochemical/antioxidant properties.     

虎杖提取物对CCl_4诱导的小鼠急性肝损伤的保护作用

目的观察虎杖提取物对CCl4诱导的小鼠急性肝损伤的保护作用。方法采用CCl4诱导小鼠急性肝损伤模型,测定血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、肝组织超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量。结果 CCl4诱导的小鼠急性肝损伤模型,血清ALT、AST明显升高,肝组织SOD活性明显降低,MDA含量显著升高（P〈0.01）;虎杖提取物能显著降低血清ALT,AST,明显提高肝组织SOD活性,降低肝组织MDA含量（P〈0.01）。结论虎杖提取物具有降酶及抗氧化的作用,对CCl4诱导的小鼠急性肝损伤具有一定的保护作用。     

虎杖提取物对小鼠急性肝损伤的保护作用

目的观察虎杖提取物对cch诱导的小鼠急性肝损伤的保护作用。方法采用CCl4诱导小鼠急性肝损伤模型,测定血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AsT）、肝组织超氧化物歧化酶（S（）D）活性及丙二醛（MDA）含量。结果cch诱导的小鼠急性肝损伤摸型,血清ALT、AST明显升高,肝组织SOD活性明显降低,MDA含量显著升高（P〈0．01）;虎杖提取物能显著降低血清ALT,AST,明显提高肝组织SOD活性,降低肝组织MDA含量（P〈0．01）。结论虎杖提取物具有降酶及抗氧化的作用。对CCh诱导的小鼠急性肝损伤具有一定的保护作用。