The comparison of antioxidative and hepatoprotective activities of Codonopsis pilosula polysaccharide (CP) and sulfated CP

Codonopsis pilosula polysaccharide (CP) was extracted, purified and modified by chlorosulfonic acid-pyridine method to obtain a sulfated CP (sCP). Their antioxidative activities in vitro were compared through the free radical-scavenging test. The results demonstrated that the scavenging capabilities of sCP were significantly stronger than those of CP. In vivo test, the mice hepatic injury model was prepared by BCG/LPS method, then administrated respectively with sCP and CP at three dosages, the biochemical indexes in serum, antioxidative indexes in liver homogenate and histopathological change in liver of the mice were compared. The results showed that in high (200 mg/kg) and middle (150 mg/kg) dosages of sCP groups, the contents of ALT, AST and TNF-α in serum and MDA in liver homogenate were significantly lower than those in the model group and numerically lower than those in the CP groups, the activities of SOD and GSH-Px in liver homogenate were significantly higher than those in the model group and numerically higher than those in the CP groups. In the model group there were obvious pathological changes in the liver, while in the sCP groups were near normal. These results indicate that sCP and CP possess antioxidative activity in vitro and in vivo, the activity of sCP is stronger than that of CP and sulfation modification can enhance the antioxidative and hepatoprotective activities of Codonopsis pilosula polysaccharide.     

Protective effects of seabuckthorn (Hippophae rhamnoides L.) seed oil against carbon tetrachloride-induced hepatotoxicity in mice

The present study examined the protective effects of seabuckthorn (Hippophae rhamnoides L., SBT) seed oil on carbon tetrachloride (CCl₄)-induced hepatic damage in male ICR mice. Our results showed that oral administration of SBT seed oil at doses of 0.26, 1.30, and 2.60 mg/kg for 8 weeks significantly reduced the elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), triglyceride (TG), and cholesterol at least 13% in serum, and the level of malondialdehyde (MDA) in liver at least 22%, that was induced by CCl₄ (1 mL/kg) in mice. Moreover, the treatment of SBT seed oil was also found to significantly increase the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Rd), and GSH content in liver up to 134%. Our study found that the optimal dose of SBT seed oil was 0.26 mg/kg, as the minimum amount exhibiting the greatest hepatoprotective effects on CCl₄-induced liver injury. Overall, the hepatoprotective effect of SBT seed oil at all tested doses was found to be comparable to that of silymarin (200 mg/kg) and have been supported by the evaluation of the liver histopathology in mice.     

Medium optimization and potential hepatoprotective effect of mycelial polysaccharides from Pholiota dinghuensis Bi against carbon tetrachloride-induced acute liver injury in mice

Response surface methodology was employed to optimize the medium compositions for the production of mycelial polysaccharide from Pholiota dinghuensis Bi (PDP). As a result, the optimal medium for crude PDP production was determined as follows (g/L): glucose 36.0, corn flour 11.8, peptone 3.0, yeast extract 5.4, KH₂PO₄ 1.0, and MgSO₄ 1.5. In a verification experiment, a yield of 756 ± 38 mg/L crude PDP was obtained. Furthermore, biochemical assay and histopathological analysis showed that crude PDP exerted significant hepatoprotective effect in a dose-dependent manner against carbon tetrachloride (CCl₄)-induced acute liver injury. Crude PDP prevented the increase of activities of serum alanine aminotransferase and aspartate aminotransferase, reduced the formation of malondialdehyde and enhanced the activities of superoxide dismutase and glutathione peroxidase in CCl₄-induced hepatotoxicity in mice.     

The NF-κB inhibitor celastrol attenuates acute hepatic dysfunction induced by cecal ligation and puncture in rats

Acute hepatic dysfunction associating sepsis is mediated mainly by toll-like receptor-4 (TLR-4)/nuclear factor kappa‐B (NF-κB) inflammatory pathway. This study explores potential hepatoprotective effect of the NF-κB inhibitor celastrol in cecal ligation and puncture (CLP) model in rats.Protective effect of celastrol (1 mg/kg, i.p., 1 h before CLP) was illustrated after 24 h by preventing CLP‐induced hepatic histopathological changes and elevation in serum hepatic biomarkers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TB) and gamma aminotransferase (γ-GT)] without affecting mortality. Celastrol anti‐inflammatory effect was illustrated by inhibiting increased serum and hepatic mRNA expression of interleukin-6 (IL-6) without affecting IL-10 elevation. Furthermore, celastrol inhibited CLP-induced elevations in hepatic mRNA expression of nuclear factor inhibitory protein kappa-B alpha (NFκBia), TLR-4, 5‐lipoxygenase (5-LOX) and prevented NF‐κB/p65 nuclear translocation and activation.In conclusion, celastrol prevented CLP-induced acute hepatic dysfunction through its anti-inflammatory effect by attenuating NF-κB activation, TLR-4 and 5-LOX expression with subsequent reduction in pro-inflammatory IL-6.     

Hepatoprotective activities of two Ethiopian medicinal plants

The present study evaluated the in vivo hepatoprotective activity of two medicinal plants, namely, Justicia schimperiana (Hochst. ex Nees) (Acanthaceae) and Verbascum sinaiticum Benth. (Scrophulariaceae) used in Ethiopian traditional medical practices for the treatment of liver diseases. The levels of hepatic marker enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were used to assess their hepatoprotective activity against carbon tetrachloride (CCl₄)-induced hepatotoxicity in Swiss albino mice. The results revealed that pretreating mice with the hydro-alcoholic extracts of both plants significantly suppressed the plasma AST ((P?<?0.01) J. schimperiana; (P?<?0.05) V. Sinaiticum) and ALT ((P?<?0.05) J. schimperiana) activity when compared with the CCl₄ intoxicated control. Among the Soxhlet extracts of each of the plants, the methanol extract of J. schimperiana showed significant hepatoprotective activity. Further fractionation of this extract using solid phase extraction and testing them for bioactivity indicated that the fractions did not significantly reverse liver toxicity caused by CCl₄. However, the percentage hepatoprotection of the distilled water fraction was comparable with that of the standard drug silymarin at the same dose (50?mg/kg) as evidenced by biochemical parameters. Histopathological studies also supported these results. In vitro DPPH assay conducted on the water fraction of J. schimperiana and the Soxhlet methanol fraction of V. sinaiticum showed that they possess moderate radical scavenging activity (IC₅₀?=?51.2 and 41.7 μg/mL, respectively) which led to the conclusion that the hepatoprotective activity of the plants could be in part through their antioxidant action.     

Ameliorative influence of Urtica dioica L against cisplatin-induced toxicity in mice bearing Ehrlich ascites carcinoma

Cisplatin (CP) is a widely used cytotoxic agent against cancer, and high doses of CP have been known to cause nephrotoxicity and hepatotoxicity. Some reports claim that antioxidants can reduce CP-induced toxicity. This study investigated the hepatoprotective, nephroprotective, and antioxidant activity of Urtica dioica L methanolic extract (UDME) against CP toxicity in Erhlich ascites tumor (EAT)-bearing mice. Levels of serum hepatic enzymes, renal function markers, and oxidant/antioxidant parameters of liver tissue were measured. Mice were inoculated with EAT on day 0 and treated with nothing else for 24 hours. After a single dose of CP administration on day 1, the extract was given at the doses of 50, 100, 200, and 400?mg/kg body weight daily during 6 days. Almost all doses of UDME performed a significant (P?<?0.05) preventive role against CP toxicity by decreasing aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, blood urea nitrogen, creatinine, lipid peroxidation, protein oxidation levels, and myeloperoxidase activity, as well as increasing reduced glutathione content, superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase activities. This suggests that UDME has a protective capacity and antioxidant activity against CP toxicity in EAT-bearing mice, probably by promoting antioxidative defense systems.     

Hepatoprotective activity of Chhit-Chan-Than extract powder against carbon tetrachloride-induced liver injury in rats

The capability of Chhit-Chan-Than extract powder (CCTEP, 10% aqueous Ocimum gratissimum L. extract) to protect against carbon tetrachloride (CCl₄)-induced oxidative stress and hepatotoxicity in vivo was investigated. Wistar rats were divided into five groups. Group A was a normal control group given only vehicle; Group B, the hepatotoxic group, was injected intraperitoneally twice a week with repeated 8% CCl₄/olive oil (0.1 mL/100 g of body weight); Groups C–E, extract-treated groups received CCl₄ and different doses of CCTEP (100 mg/kg and 200 mg/kg) or silymarin (200 mg/kg of body weight) daily by gavage for 8 weeks, respectively. The results showed that the CCl₄-induced histopathogical changes may be prevented by CCTEP through reducing the intercellular collogen stack, dropping blood serum alanine aminotransferase and aspartate aminotransferase levels, and restoring the catalase activity and glutathione content. The hepatoprotective properties were further confirmed by the marked improvement in histopathological examination and by quantitative steatosis-fibrosis scoring. The above results suggest that CCTEP is able to prevent the liver inflammation and fibrosis induced by repeated CCl₄ administration, and the hepatoprotective effects might be correlated partly with its antioxidant and free radical scavenging effects.     

中药复方JEYS对小鼠急性肝损伤的保护作用

目的观察中药复方JEYS（TCCJEYS）的保肝作用及作用机制。方法建立D-半乳糖胺（D-GalN）诱导的小鼠急性肝损伤模型,观察TCCJEYS的保肝作用及作用机制。结果 TCCJEYS能够显著降低肝脏指数（LI）、谷丙转氨酶（ALT）、谷草转氨酶（AST）活力和丙二醛（MDA）含量,显著升高超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活力,促进肝组织中B细胞淋巴瘤/白血病-2（Bcl-2）蛋白的表达和抑制自杀相关因子（Fas）蛋白的表达,HE染色也显示TCCJEYS组病变程度比模型组轻。结论 TCCJEYS对D-GalN诱导的小鼠急性肝损伤具有保护作用。     

Antioxidant and hepatoprotective activities of Egyptian moraceous plants against carbon tetrachloride-induced oxidative stress and liver damage in rats

Context: In the absence of reliable liver-protective drugs in modern medicine, a large number of medicinal preparations are recommended for treatment of liver disorders.

Objective: The antioxidant, hepatoprotective and kidney protective activities of methanol extracts of Ficus carica Linn. (Moraceae) leaves and fruits and Morus alba Linn. root barks (Moraceae) are evaluated here.

Materials and methods: Liver and kidney damage were induced in rats by carbon tetrachloride in a subcutaneous dose of 1?mL (40% v/v in corn oil)/kg. The extract was given intraperitoneally at doses of 50?mg/kg (F. carica leaf and M. alba root bark) and 150?mg/kg (F. carica fruit). The activity of the extracts was comparable to that of silymarin, a known hepatoprotective agent. Antioxidant activity was evaluated by measuring blood glutathione (GSH) content, superoxide dismutase (SOD), catalase (CAT) activities, and malondialdehyde equivalent (MDA). Hepatoprotective activity was evaluated by measuring serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, and total protein. These biochemical observations were supported by histopathological examination of liver sections. Kidney function was evaluated by measuring plasma urea and creatinine.

Results: Methanol extracts of Ficus carica and Morus alba showed potent antioxidant and hepatoprotective activities; in-depth chromatographic investigation of the most active extract (Ficus carica leaf extract) resulted in identification of umbelliferone, caffeic acid, quercetin-3-O-β-d-glucopyranoside, quercetin-3-O-α-l-rhamnopyranoside, and kaempferol-3-O-α-l-rhamnopyranoside.

Discussion and conclusion: These findings demonstrate that the phenolic constituents of Ficus carica leaf and Morus alba root bark are responsible at least in part for the observed protective effects.     

8-甲氧补骨脂素对对乙酰氨基酚致小鼠急性肝损伤的保护作用

目的研究8-甲氧补骨脂素(8-methoxypsoralen,8-MOP)对对乙酰氨基酚(acetaminophen,APAP)致小鼠急性肝损伤的保护作用。方法采用对乙酰氨基酚所致小鼠急性肝损伤模型。24 h后,检测小鼠血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)和乳酸脱氢酶(LDH);留取肝脏组织,常规石蜡包埋切片,HE染色,光镜观察肝脏组织病理变化;制备肝匀浆,测定肝中还原型谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)和丙二醛(MDA)的含量。结果与正常对照组比较,模型组小鼠血清中ALT、AST和LDH活性明显升高,肝脏组织出现明显的肝细胞变性坏死;与模型组相比,8-甲氧补骨脂素可以明显降低小鼠血清中ALT、AST和LDH的活性,降低肝组织中MDA的含量,升高GSH/GSSG比值,肝组织病理损伤也明显减轻。结论 8-甲氧补骨脂素对对乙酰氨基酚致小鼠急性肝损伤具有明显的保护作用。     

Protective effect of cactus (Opuntia ficus indica) cladode extract upon nickel-induced toxicity in rats

The purpose of this study carried out on male Wistar rats, was to evaluate the protective effects of regular ingestion of juice from the prickly pear cactus (Opuntia ficus indica) cladodes against nickel chloride toxicity. Rats were given either normal tap water or water containing 25% of cactus juice for one month. Then, rats of each group were injected daily, for 10 days, with either NiCl₂ solution (4 mg (30 μmol)/kg body weight) or with the same volume of saline solution (300 mM NaCl).Significant increases of lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase activities and of cholesterol, triglycerides and glucose levels were observed in blood of nickel-treated rats. In the liver, nickel chloride was found to induce an oxidative stress evidenced by an increase in lipid peroxidation and changes in antioxidant enzymes activities. Superoxide-dismutase (SOD) activity was found to be increased whereas glutathione peroxidase and catalase activities were decreased. These changes did not occur in animals previously given cactus juice, demonstrating a protective effect of this vegetal extract.     

Protective effect of Woodfordia fruticosa flowers against acetaminophen-induced hepatic toxicity in rats

Context: The flowers of Woodfordia fruticosa Kurz. (Lythraceae) are commonly used for the treatment of several ailments which includes rheumatism, leucorrhea, menorrhagia, asthma, liver disorder, and inflammatory conditions.

Objective: To evaluate the hepatoprotective property of Woodfordia fruticosa flowers against acetaminophen-induced hepatic injury in rats.

Material and methods: Acetaminophen (3?g/kg bw)-induced hepatotoxicity study was carried out by observing the effect of methanol extract of Woodfordia fruticosa flowers (400 and 600?mg/kg, bw) on some serum marker enzymes, albumin, blood urea nitrogen levels as well as liver total protein, nonenzymetic glutathione reduced content, and enzymatic antioxidant glutathione peroxidase, with histopathological evidence.

Results and discussion: Pretreatment of rats with methanol extract of Woodfordia fruticosa flowers effectively prevented the acetaminophen-induced hepatic damage as indicated by the serum marker enzymes aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase and other biochemical parameters (albumin and blood urea nitrogen). Parallel to these changes, the methanol extract of Woodfordia fruticosa flowers also prevented acetaminophen-induced oxidative stress in the rat liver by inhibiting depletion of liver total protein and restoring the levels of nonenzymatic antioxidant glutathione reduced. The biochemical changes were consistent with histopathological observations suggesting marked hepatoprotective effect of the methanol extract of Woodfordia fruticosa flowers.

Conclusion: The results suggested that methanol extract of Woodfordia fruticosa flowers possesses protective effect against acetaminophen-induced hepatotoxicity.     

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.     

Hepatoprotective properties of Morinda pubescens J.E. Smith (Morinda tinctoria Roxb.) fruit extract

The present study evaluated the hepatoprotective properties of Morinda pubescens fruit extract against d-galactosamine (d-GalN)-induced liver injury in rats. The fruit extract of M. pubescens was administrated orally at 200 mg/kg of body weight daily once for 21 days and at 21st day, d-GalN (500 mg/kg of body weight) was injected intraperitoneally in rats, to induce liver damage. In d-GalN administrated rats, significant increase in the levels of serum marker enzymes and lipid peroxidation (LPO) in liver and decreased serum and liver antioxidant levels were observed. Pre-treatment with fruit extract to rats reduced the elevated levels of serum marker enzymes and also improves the levels of fucose, ceruloplasmin, and uric acid. Administration of M. pubescens fruit extract prevented increase of LPO and alteration in iron content in experimental animals, besides, considerably increased the levels of glutathione (GSH) and vitamin E when compared to d-GalN intoxicated animals. The present results suggest that the M. pubescens fruit extract has liver-protective property against d-GalN-induced liver injury in rats, which was further confirmed by histopathological studies. The hepatoprotective potentials of fruits of M. pubescens may be due to the presence of phenols and alkaloids, as analyzed by preliminary phytochemical analysis of fruit extract.     

Comparative effects of curcumin and resveratrol on aflatoxin B1-induced liver injury in rats

Aflatoxin B₁ is a potent hepatotoxic and hepatocarcinogenic mycotoxin. Lipid peroxidation and oxidative DNA damage are the principal manifestations of aflatoxin B₁-induced toxicity that could be counteracted by antioxidants. Many plant constituents have been reported to prevent liver damage associated with lipid peroxidation. In this study, curcumin (polyphenolic antioxidant purified from turmeric) and resveratrol (polyphenol obtained from grapes) were evaluated for possible protection against liver injury induced by aflatoxin B₁ in rats. Adult male Fischer rats were divided into six groups including untreated control, curcumin control (200 mg/kg BW), resveratrol control (10 mg/kg BW) and aflatoxin B₁ (25 μg/kg BW). Other two groups were administered either curcumin or resveratrol along with aflatoxin B₁. The study was carried out for 90 days. At the end of the experiment period, blood and tissue samples were collected from the animals before they were killed. Livers were collected for histopathologic studies and fixed in 10% buffered formalin solution. Serum was used for estimation of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and γ-glutamyl transferase (γ-GT) enzymes. The lipid peroxidation, reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated in liver homogenates. The results revealed that aflatoxin B₁ administration caused liver damage as indicated by statistically significant (P < 0.05) increase in serum ALT, AST and γ-GT levels. In addition, there were general statistically significant reductions in the activities of GSH, SOD, CAT, GSH-Px, and an increase in lipid peroxidation in the liver of aflatoxin B₁-treated group compared to the untreated control group. Curcumin showed a significant hepatoprotective activity by lowering the levels of serum marker enzymes, lipid peroxidation and elevating the levels of GSH, SOD, CAT and GSH-Px. However, resveratrol failed to protect from the aflatoxin B₁-induced liver injury. These findings suggest that curcumin but not resveratrol has a hepatoprotective effect against aflatoxin B₁-induced liver injury.     

Hepatoprotective effects of Tagetes lucida root extract in carbon tetrachloride-induced hepatotoxicity in Wistar albino rats through amelioration of oxidative stress

ContextThe roots of Tagetes lucida Cav. (Asteraceae) have antioxidant and antimicrobial properties.ObjectiveThis study aimed to examine the hepatoprotective effects of T. lucida roots ethanol extract (TLRE) using carbon tetrachloride (CCl₄)-induced hepatotoxicity in rats.Materials and methodsThe active ingredients of TLRE were identified by high-performance liquid chromatography, infra-red spectrum, and mass spectrometric procedures. Ninety rats were distributed into four main groups: positive, therapeutic, protective, and negative group. The therapeutic group was implemented using CCl₄ (a single dose of 2 mL/kg) before TLRE or silymarin administration. Meanwhile, the protective group was implemented by administering CCl₄ (a single dose of 2 mL/kg) after force-feeding TLRE or silymarin. Each therapeutic and protective group was divided into three subgroups: force-fed with saline, TLRE (500 mg/kg), and silymarin (25 mg/kg). The positive group was split into two subgroups that were force-fed TLRE and silymarin. Positive, therapeutic, and protective groups were compared to the negative group (untreated rats). CCl_4, TLRE, and silymarin were orally administrated using a gastric tube.ResultsIn the therapeutic and protective groups, TLRE significantly reduced liver enzymes, i.e., aspartate aminotransferase (12.47 and 6.29%), alanine aminotransferase (30.48 and 11.39%), alkaline phosphatase (17.28 and 15.90%), and cytochrome P450-2E1 (39.04 and 48.24%), and tumour necrosis factor-α (53.72 and 53.72%) in comparison with CCl₄-induced hepatotoxicity controls.ConclusionsTLRE has a potent hepatoprotective effect with a good safety margin. After a repeated study on another type of small experimental animal, their offspring, and an experiment with a large animal, this study may lead to clinical trials.     

Hepatoprotective and antioxidant activity of Leucas aspera against d-galactosamine induced liver damage in rats

Context: Whole plant of Leucas aspera (LA) Willd. (Labiatae) is traditionally used in Siddha medicine for hepatic ailments.

Objective: LA was investigated for its hepatoprotective, antioxidant, and protective effect on microsomal drug metabolizing enzymes (MDMEs).

Materials and methods: LA aqueous extract (200 and 400 mg/kg, p.o.) was evaluated for its hepatoprotective and antioxidant activity in d-galactosamine (d-GalN)-induced hepatotoxicity in rats. Biochemical and histopathological studies were performed to assess hepatoprotective activity. Hexobarbitone-induced sleeping time model was used to study the protective effect of LA on MDMEs.

Results: d-GalN administration induced hepatotoxicity in rats which was manifested by increased levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total cholesterol, triglycerides, total bilirubin and oxidative stress. Pretreatment with LA extract significantly protected the liver in d-GalN administered rats. LA extract significantly elevated antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase and decreased lipid peroxidation levels in liver. The total phenolic and flavonoid content in LA aqueous extract was found to be 28.33 ± 0.19 gallic acid equivalents mg/g of extract and 3.96 ± 0.57 rutin equivalent mg/g of extract, respectively. LA extract (200 and 400 mg/Kg) treatment with CCl₄ decreased the hexobarbitone-induced sleeping time in mice by 56.67 and 71.30%, respectively, which indicated the protective effect of LA on hepatic MDMEs. Histological studies showed that LA at 400 mg/kg attenuated the hepatocellular necrosis in d-GalN intoxicated rats.

Conclusion: Our results contribute towards validation of the traditional use of LA in hepatic disorders.     

Protective effects of Salvia plebeia compound homoplantaginin on hepatocyte injury

Salvia plebeia R. Br is a traditional Chinese herb which has been considered as an inflammatory mediator used for treatment of many infectious diseases including hepatitis. Previously, the compound homoplantaginin was isolated in our group. Hence, we evaluated the protective effects of homoplantaginin on hepatocyte injury. Homoplantaginin displayed an antioxidant property in a cell-free system and showed IC₅₀ of reduction level of DPPH radical at 0.35 μg/ml. In human hepatocyte HL-7702 cells exposed to H₂O₂, the addition of 0.1–100 μg/ml of homoplantaginin, which did not have a toxic effect on cell viability, significantly reduced lactate dehydrogenase (LDH) leakage, and increased glutathione (GSH), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in supernatant. In vivo assay, we employed the model of Bacillus Calmette–Guérin (BCG)/lipopolysaccharide (LPS)-induced hepatic injury mice to evaluate efficacy of homoplantaginin. Homoplantaginin (25–100 mg/kg) significantly reduced the increase in serum alanine aminotranseferase (ALT) and aspartate aminotransferase (AST), decreased the levels of tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1). The same treatment also reduced the content of thiobarbituric acid-reactive substances (TBARS), elevated the levels of GSH, GSH-Px and SOD in hepatic homogenate. The histopathological analysis showed that the grade of liver injury was ameliorated with reduction of inflammatory cells and necrosis of liver cells in homoplantaginin treatment mice. These results suggest that homoplantaginin has a protective and therapeutic effect on hepatocyte injury, which might be associated with its antioxidant properties.     

Hepatoprotective potential of polyphenol rich extract of Murraya koenigii L.: an in vivo study

The present study investigates hepatoprotective effects of polyphenol rich Murraya koenigii L. (MK) hydro-ethanolic leaf extract in CCl(4) treated hepatotoxic rats. Plasma markers of hepatic damage, lipid peroxidation levels, enzymatic, and non-enzymatic antioxidants in liver and histopathological changes were investigated in control and treated rats. MK pretreated rats with different doses (200, 400 and 600mg/kg body weight) showed significant decrement in activity levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total protein, and bilirubin. Also, MK treated rats recorded a dose dependent increment in hepatic super oxide dismutase, catalase, reduced glutathione and ascorbic acid and, a decrement in lipid peroxidation. Microscopic evaluations of liver revealed CCl(4)-induced lesions and related toxic manifestations that were minimal in liver of rats pretreated with MK extract. These results demonstrate that hydro-ethanolic leaf extract of MK possesses hepatoprotective potentials.     

Hepatoprotective effects of Juglans regia extract against CCl4-induced oxidative damage in rats

Abstract

Context: Different parts of the walnut [Juglans regia L. (Juglandaceae)] have been used in folk medicine for protection against liver injury, although its actual efficacy remains uncertain.

Objective: The present study investigated the protective effect of walnut leaf extract against carbon tetrachloride (CCl₄)-induced liver damage in rats.

Materials and methods: The rats were randomly divided into seven groups: control, CCl₄ (i.p., 0.5?mL/kg b.w., 50% CCl₄ in olive oil), walnut extract (at dose level of 0.2?g/kg b.w.) alone, walnut extract (at dose levels of 0.05, 0.1, 0.2 and 0.4?g/kg b.w.) with CCl₄, and treatment was carried out accordingly. On the 28th day, rats were sacrificed and blood was withdrawn by cardiac puncture. Liver damage was assessed by serum biochemical parameters (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and albumin), antioxidant enzymes (superoxide dismutase and catalase) and histopathological observation.

Results: Administration of walnut leaf extract (ranging from 0.2 to 0.4?g/kg b.w.) significantly lowered serum alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase levels in CCl₄-treated rats. Walnut leaf extract increased antioxidant enzymes, including superoxide dismutase and catalase. Histopathological examination of livers showed that walnut leaves extract reduced fatty degeneration, cytoplasmic vacuolization and necrosis in CCl₄-treated rats.

Discussion and conclusion: These results suggest that walnut extract has a protective effect over CCl₄-induced oxidative damage in rat liver. These results demonstrate that walnut extract acts as a good hepatoprotective and antioxidant agent in attenuating hepatocellular damage.