Protective effect of Nigella sativa seeds against carbon tetrachloride-induced liver damage

It has been reported that Nigella sativa oil possesses hepatoprotective effects in some models of liver toxicity. However, it is N. sativa seeds that are used in the treatment of liver ailments in folk medicine rather than its oil. Therefore, the aim of this study was to investigate the effect of the aqueous suspension of N. sativa on carbon tetrachloride (CCL4)-induced liver damage. Aqueous suspension of the seeds was given orally at two dose levels (250 mg/kg and 500 mg/kg) for five days. CCL4 (250 microl/kg intraperitoneally / day in olive oil) was given to the experimental group on days 4 and 5, while the control group was only treated with the vehicles. Animals treated with CCL4 showed remarkable centrilobular fatty changes and moderate inflammatory infiltrate in the form of neutrophil and mononuclear cells when compared to the controls. This effect was significantly decreased in animals pretreated with N. sativa. Histopathological or biochemical changes were not evident following administration of N. sativa alone. Serum levels of aspartic transaminase (AST), and L-alanine aminotransferase (ALT) were slightly decreased while lactate dehydrogenase (LDH) was significantly increased in animals treated with CCL4 when compared to the control group. LDH was restored to normal but ALT and AST levels were increased in animals pretreated with N. sativa. In conclusion, N. sativa seeds appeared to be safe and possibly protective against CCL4-induced hepatotoxicity. However, further studies may still be needed prior to supporting its use in folk medicine for hepatic diseases.     

金丝桃苷对小鼠急性酒精性肝损伤的保护作用

目的:研究金丝桃苷对乙醇致小鼠急性酒精性肝损伤的保护作用。方法:昆明种小鼠随机分为正常组、模型组、联苯双脂组(5.625 mg/kg)和金丝桃苷(12.5、25、50 mg/kg)剂量组。每日灌胃给药1次,连续7 d。末次给药1 h后,除正常组外,分别灌胃给予50%乙醇14 ml/kg复制酒精性肝损伤模型。复制模型12 h后,处理动物,测定小鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)和γ-谷氨酰转移酶(GGT)以及甘油三酯(TG)和胆固醇(TC)水平;测定肝组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)和谷胱甘肽(GSH)含量。苏木素-伊红(HE)染色,观察肝组织病理学变化。结果:与正常组比较,模型组小鼠清ALT,AST,GGT及TG水平显著升高,肝组织SOD活性及GSH含量显著降低,MDA含量显著升高,病理学结果显示模型组肝组织损伤明显。与模型组比较,金丝桃苷(25、50 mg/kg)剂量组均能降低血清中ALT、AST,GGT和TG水平以及肝组织中MDA含量,同时升高SOD活性和GSH含量;金丝桃苷(12.5 mg/kg)剂量组能降低血清中ALT、AST水平,升高SOD活性;金丝桃苷各剂量组(12.5、25、50 mg/kg)均能减轻肝损伤的病变程度。结论:金丝桃苷对乙醇所致的小鼠急性酒精性肝损伤具有保护作用,其机制可能与抗氧化作用和抑制脂质过氧化损伤有关。     

灯盏花素对四氯化碳小鼠肝损伤的保护作用

目的探讨灯盏花素对四氯化碳(CCl4)肝脏损伤的保护作用.方法小鼠腹腔注射0.1% CCl4 10ml/kg 造成肝损伤模型,以血清丙氨酸氨基转移酶(ALT)、肝匀浆谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量为指标观察灯盏花素对肝脏损伤的保护作用.结果灯盏花素50mg、100mg/kg·d ig×7d能明显降低CCl4中毒小鼠的血清ALT含量和肝匀浆MDA含量,提高肝脏GSH-Px活性.结论灯盏花素具有明显的保护肝作用,可通过增强抗氧化能力拮抗四氯化碳的肝毒性.     

Trianthema portulacastrum affords antihepatotoxic activity against carbon tetrachloride-induced chronic liver damage in mice: reflection in subcellular levels

The efficacy of an ethanol extract of Trianthema portulacastrum as a hepatoprotective agent was investigated against carbon tetrachloride (CCl₄)-induced chronic liver injury in mice. The CCl₄ was administered per os (p.o.) three times a week for 5 weeks. Daily administration (p.o.) of T. portulacastrum plant extract at 100 or 150 mg/kg was started 2 weeks before the commencement of CCl₄ treatment and it continued during the entire period of the treatment. The extract dose-dependently decreased the activities of serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, alkaline phosphatase, glutamate dehydrogenase and sorbitol dehydrogenase as well as serum levels of bilirubin and urea which were otherwise significantly elevated with the chronic CCl₄ regimen alone. There was a substantial increase in the activities of plasma membrane enzymes γ-glutamyl transpeptidase and 5′-nucleotidase and lysosomal enzymes acid phosphatase and acid ribonuclease in hepatic tissue following CCl₄ treatment. These changes were reversed towards normalization with the extract in a dose-dependent manner. The extract also restored CCl₄-induced inhibition of hepatic microsomal enzyme glucose-6-phosphatase. The activities of mitochondrial succinate dehydrogenase and adenosine 5′-triphosphatase which were significantly attenuated by CCl₄ administration remained unaltered following the extract therapy. Results of this study provide evidence that the extract possesses a marked liver protective action which is comparable to that of silymarin, a standard hepatoprotective drug. The probable mechanism by which this plant exerts cytoprotection has also been discussed. © 1997 John Wiley & Sons, Ltd.     

Protective effects of hyperoside against human umbilical vein endothelial cell damage induced by hydrogen peroxide

Ethnopharmacological relevance

Hyperoside (Hyp) is a flavonoid compound isolated from Rhododendron ponticum L. leaves that elicits vascular protective effects in vitro. Treatment with Hyp has been found to attenuate endothelial cell damage induced by oxidative stress, but its mechanisms of action remain unclear.This study investigated the action of Hyp in an endothelial injury model induced by hydrogen peroxide (H₂O₂), as well as its possible mechanisms.

Materials and methods

Human umbilical vein endothelial cells (HUVECs) were treated with H₂O₂ alone or in combination with Hyp. The protective effects of Hyp against H₂O₂ were evaluated, and the activation of extracellular signal-regulated protein kinase (ERK) in Hyp was assayed in HUVECs.

Results

Loss of cell viability as well as excessive cell apoptosis and death were observed in HUVECs after 18 h of challenge with H₂O₂ (400 μM); however, both cell apoptosis and death were attenuated in the Hyp-pretreated cells. Western blot analysis revealed that Hyp increased the expression of Bcl-2 but decreased that of Bax. In addition, Hyp induced the phosphorylation of ERK1/2 in HUVECs.

Conclusion

These observations provide preliminary evidence that Hyp protects HUVECs against H₂O₂ damage, at least partially, by activating the ERK signaling pathway.     

Evaluation of hepatoprotective effects of Helminthostachys zeylanica (L.) Hook against carbon tetrachloride-induced liver damage in Wistar rats

The rhizomes of Helminthostachys zeylanica (L.) are used by the Kattunaikan tribe of Kerala, for the treatment of various hepatic disorders. In the present study, the effect of the methanolic extract of Helminthostachys zeylanica rhizomes on carbon tetrachloride (CCl4)-induced liver damage in Wistar rats was studied. The results showed that significant hepatoprotective effect was obtained against CCl4-induced liver damage, by oral administration of Helminthostachys zeylanica methanolic extract as evident from decreased levels of serum enzymes and an almost normal architecture of the liver, in the treated groups, compared to the controls. The extract was effective in increasing the choleretic activity of anaesthetised normal rats. It also shortened hexobarbitone-induced sleeping time in mice, which was increased by CCl4 treatment, besides showing significant antilipid peroxidant effect in vitro. Thus, the present study provides a scientific rationale for the traditional use of this plant in the management of liver diseases.     

Protective effects of luteolin against apoptotic liver damage induced by D-galactosamine/lipopolysaccharide in mice

In this study, the protective effects of luteolin (1, a major component of Cirsium japonicum) were examined against d-galactosamine (GalN)/lipopolysaccharide (LPS)-induced fulminant hepatic failure. Mice received an intraperitoneal injection of 1 (25, 50, 100, and 200 mg·kg(-1)) 1 h before treatment with GalN (700 mg·kg(-1))/LPS (10 μg·kg(-1)). Treatment with GalN/LPS resulted in increased mortality and serum aminotransferase activity. These increases were attenuated by pretreatment with 1. Treatment with GalN/LPS induced an increase in the serum level of tumor necrosis factor-α (TNF-α) and protein expression of TNF-α receptor-associated death domain, and these increases were prevented by 1. In addition, 1 attenuated apoptosis induced by GalN/LPS treatment, which was analyzed using a caspase-3 and -8 activity assay, as well as by proapoptotic BH3-only protein and cytochrome c protein expression, and by a terminal deoxynuleotidyl transferase-mediated dUTP nick end-labeling method. After GalN/LPS injection, nuclear phosphorylated c-Jun levels showed a significant increase, which were attenuated by 1. The present findings suggest that luteolin ameliorates D-GalN/LPS-induced liver injury and that this protection is likely due to inhibition of the extrinsic and intrinsic apoptotic pathways.     

Antifibrotic activity of Taraxacum officinale root in carbon tetrachloride-induced liver damage in mice

Aim of the study

Dandelion (Taraxacum officinale) has been traditionally used in the treatment of various liver disorders. The present study was aimed to assess the efficacy of dandelion root water–ethanol extract (DWE) in carbon tetrachloride (CCl₄)-induced hepatic fibrosis.

Materials and Methods

The mice were treated with CCl₄ dissolved in olive oil (20%, v/v, 2 ml/kg) intraperitoneally (i.p.), twice a week for 4 weeks. DWE was administered i.p. once daily for next 10 days, in doses of 200 and 600 mg/kg of body weight. The degree of hepatic fibrosis was determined by hydroxyproline content and Mallory trichrome staining. Oxidative stress was determined by measuring hepatic superoxide dismutase (Cu/Zn SOD) activity. The expression and specific tissue distribution of glial fibrillary acidic protein (GFAP), alpha-smooth muscle actin (α-SMA), and metallothionein (MT) I/II in the liver were determined by immunohistochemistry.

Results

Hepatic Cu/Zn SOD activity has been decreased in intoxicated mice and normalized in DWE treated groups. MT I/II immunopositivity was strongly reduced in the CCl₄ group. DWE treatment successfully decreased hepatic fibrinous deposits, restored histological architecture, and modulate the expression of GFAP and α-SMA. Concomitantly, MT I/II expression increased in the DWE treated groups.

Conclusions

Our results suggest the therapeutic effect of DWE on CCl₄-induced liver fibrosis by the inactivation of hepatic stellate cells and the enhancement of hepatic regenerative capabilities. The present results provide scientific evidence to substantiate the traditional use of Taraxacum officinale root in hepatic disorders.     

人参果花青素对对乙酰氨基酚致小鼠肝损伤的保护作用

目的探讨人参果花青素(ginseng fruit anthocyanins,GFA)对对乙酰氨基酚(acetaminophen,AP)致小鼠急性肝损伤的保护作用及其机制。方法建立AP诱导的肝损伤模型,观察GFA对肝损伤的保护作用。将ICR小鼠随机分为对照组、模型组(AP 250 mg/kg)和GFA低、高剂量(200、400 mg/kg)组。通过计算脏器指数,检测血清中的丙氨酸转移酶(ALT)、天冬氨酸转移酶(AST)及肝组织匀浆中的丙二醛(MDA)、谷胱甘肽(GSH)水平,结合肝组织切片来观察病理学变化。结果与模型组相比,GFA低、高剂量明显抑制了血清中ALT、AST和匀浆中MDA水平的升高,同时缓解了肝组织匀浆中GSH水平的降低(P0.05);组织病理学HE和Hoechst 33258染色显示GFA可明显改善肝组织的坏死和凋亡,并且缩小了坏死区域,减轻了细胞炎性浸润;通过炎症因子诱导型一氧化氮合酶(i NOS)、环氧化酶-2(COX-2)免疫组织化学染色和硝化应激指标3-硝基络氨酸(3-NT)免疫荧光的表达,说明GFA能够抑制硝化应激和炎症反应。结论 GFA对AP诱导的急性肝损伤有一定的保护作用,其机制可能与其抗氧化作用、抑制硝化应激、减少炎症反应及抑制细胞凋亡有关。     

Protective effects of dehydrocavidine on carbon tetrachloride-induced acute hepatotoxicity in rats

AIM OF THE STUDY: To investigate the protective effects of dehydrocavidine (DC), a main active ingredient of Corydalis saxicola Bunting (Yanhuanglian), on carbon tetrachloride (CCl4)-induced hepatotoxicity and the possible mechanisms involved in male Sprague-Dawley rats. MATERIALS AND METHODS: Acute hepatotoxicity was induced by CCl4 intoxication in rats. Serum biological analysis, lipid peroxides and antioxidants estimation, histopathological studies were carried out. RESULTS: Both pre-treatment with DC prior to CCl4 administration and post-treatment with DC after CCl4 administration significantly prevented increases in serum enzymatic activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and total bilirubin (TBIL). In addition, pre- and post-treatment with DC also significantly prevented formation of hepatic malondialdehyde (MDA), depletion of glutathione peroxidase (GPx) and depression of superoxide dismutase (SOD) in the liver of CCl4-intoxicated rats. ALT, AST, LDH, ALP and TBILL levels, as well as MDA, SOD and GPx activities were unaffected in normal rats by treatment with DC alone. GST, a phase II enzyme, had no significant changes during our experiments. Histopathological changes induced by CCl4 were also significantly attenuated by DC treatment in both preventive and curative experiments. CONCLUSIONS: DC has a potent hepatoprotective effect on CCl4-induced liver injury in rats through its antioxidant activity.     

芝麻素对四氯化碳慢性肝损伤大鼠肝脏的保护作用

目的观察芝麻提取物芝麻素对四氯化碳(CC l4)慢性肝损伤大鼠肝脏的保护作用。方法将60只SD大鼠随机分为正常组、模型组、芝麻素高剂量组、芝麻素中剂量组、芝麻素低剂量组和甘利欣对照组6组,各10只,除正常组外于皮下注射40%CC l4溶液(5 mL/kg),以后每3 d予40%CC l4溶液(3 mL/kg)皮下注射造模,正常组予等容积花生油皮下注射。同时,正常组、模型组每日予0.9%氯化钠注射液1.5 mL灌胃;芝麻素高剂量组、芝麻素中剂量组、芝麻素低剂量组每日分别予9.0、3.0、1.0 mg/mL浓度芝麻素甲基纤维素悬浊液1.5 mL灌胃;甘利欣对照组每日予0.3 mg/mL甘利欣1.5 mL灌胃。8周后处死大鼠,检测血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总蛋白(TP)、白蛋白(A lb)、球蛋白(G)含量,并进行病理组织学检查。结果芝麻素高剂量组、芝麻素中剂量组大鼠血清ALT、AST活性虽然仍高于正常组,但比模型组明显降低(P0.05),且与甘利欣对照组比较差异无统计学意义(P0.05),而且芝麻素高剂量组、芝麻素中剂量组大鼠肝组织结构破坏不明显,肝细胞脂肪变性程度显著减轻,肝细胞坏死减轻,尤以芝麻素高剂量组肝组织改善显著,接近甘利欣对照组;芝麻素高剂量组、芝麻素中剂量组、芝麻素低剂量组、甘利欣对照组TP、A lb含量比较差异无统计学意义(P0.05),但均较模型组高(P0.05),与正常组比较差异无统计学意义(P0.05),6组血清G含量比较差异无统计学意义(P0.05)。结论芝麻素能改善造模大鼠肝细胞损害和坏死状况,对肝功能有保护作用,而且与剂量有一定关系。     

木犀草素对对乙酰氨基酚诱导的L02肝细胞损伤的保护作用

探讨木犀草素(luteolin,Lut)对对乙酰氨基酚(acetaminophen,APAP)诱导的L02肝细胞损伤的保护作用。CCK-8法检测Lut对L02细胞活性的影响;筛选APAP诱导L02细胞损伤的浓度及作用时间;细胞形态学、CCK-8实验和流式细胞术检测分析Lut对APAP诱导的L02细胞凋亡的影响;比色法检测细胞上清液中丙二醛(MDA)含量、谷胱甘肽(GSH)及超氧化物歧化酶(SOD)活性;RT-PCR检测凋亡相关基因Bax,Bcl-2,caspase-3的表达。结果显示Lut在2.5~40μmol·L~(-1)不影响L02细胞活性;12 mmol·L-1APAP作用于L02细胞12 h可用于建立肝细胞损伤模型。与模型组相比,Lut组细胞状态明显改善,胞体增大,贴壁能力恢复明显;细胞凋亡率明显下降;MDA含量显著下降(P0.05或P0.01),GSH和SOD活性显著提高(P0.05或P0.01),同时能够上调Bcl-2及下调Bax,caspase-3 mRNA的表达(P0.05或P0.01)。该实验证明了Lut对APAP诱导的L02细胞损伤有保护作用,其机制可能与其减轻氧化应激反应和抑制细胞凋亡有关。     

甘草次酸衍生物抗肝纤维化的实验研究

目的探讨甘草次酸衍生物(TY501)对四氯化碳(CCl_4)致小鼠肝纤维化的保护作用及其机制。方法采用经典CCl_4造模法建立小鼠肝纤维化模型,给予高、中、低剂量(45、15、5 mg/kg)TY501干预治疗,用秋水仙碱(0.36 mg/kg)作阳性对照。给药30 d后,检测各组小鼠肝功能指标、肝纤维化指标、肝组织羟脯氨酸(Hyp)和转化生长因子-β1(TGF-β1)的量,并取其肝组织进行病理学染色。结果与模型组相比,TY501各治疗组肝功能指标(ALT、AST、ALP、ALB)、肝纤维化指标(HA、LN、PCIII、CIV)及肝组织Hyp、TGF-β1的量均有不同程度改善,其中高剂量组改善作用最为明显(P0.05、0.01);肝组织病理学切片显示,给药组小鼠肝纤维化程度降低,有逆转趋势。结论 TY501对CCl_4造成的肝纤维化有明显的保护作用。     

Protective effect of Rhodiola sachalinensis extract on carbon tetrachloride-induced liver injury in rats

This study was carried out to investigate the protective effect of an aqueous extract from the root of Rhodiola sachalinensis (RSE) on liver injury induced by repetitive administration of carbon tetrachloride in rats. RSE was given orally to rats at doses of 50, 100 or 200 mg/kg throughout the carbon tetrachloride treatment for 28 days. In rats treated with carbon tetrachloride, the levels of hydroxyproline and malondialdehyde (MDA) in the liver, and serum enzyme activities were significantly increased. RSE treatment significantly reduced the levels of liver hydroxyproline and MDA, and serum enzyme activities, in accordance with improved histological findings. Immunohistological findings indicated RSE treatment inhibited hepatic stellate cell activation, which is a major step for collagen accumulation during liver injury. These data suggest that RSE protects the liver from repetitive injury induced by carbon tetrachloride in rats.     

Hepatoprotective activity of Gentiana veitchiorum Hemsl. against against carbon tetrachloride-induced hepatotoxicity in mice

AIM： To study the hepatoprotective effect of methanol extract of Gentiana veitchiorum （MGV） against CCl4-induced oxidative stress and liver injury in mice. METHOD： The acute hepatic model was developed by injection of 20% CCh in mice. ICR mice were divided into six groups, including control, CCl4, CCl4＋ silymarin, and CCl4 MGV （100, 200, and 400 mg.kg^＆-1） groups. Hepatic enzymes including AST, ALT and ALP levels in serum, and antioxidant enzymes, including SOD, CAT and GPX activity in liver tissue, were determined. Histopathological examination and Western blot analysis were performed. RESULTS： Oral administration of MGV at 200 and 400 mg.kg-1 for 15 days dose-dependently inhibited the serum elevations of AST, ALT, and ALP, and recovered the reduction of SOD, CAT, and GPX in liver tissue. Hematoxylin and eosin staining examina- tion performed in liver tissues suggested that MGV treatment ameliorated histopathological changes in CCl4-induced mice. Westem blotting analysis implied that MGV increased HO-1 expression and recovered TNF-α alternation. CONCLUSION： G veitchiorum can protect the liver against CCl4-induced damage in mice, and this hepatoprotective effect was due at least in part to its ability through scavenging CCl4-associated free radical activities. The study provided in vivo evidence that G veitchiorum can be used as a safe, cheap, and effective agent to reduce acute liver damage, supporting its folk medicine use.     

Protective effect of Lygodium flexuosum (L.) Sw. extract against carbon tetrachloride-induced acute liver injury in rats

The hepatoprotective potential of Lygodium flexuosum (L.) Sw. was evaluated in male Wistar rats against carbon tetrachloride-induced liver damage in preventive and curative models. Toxic control and n-hexane extract-treated rats received a single dose of CCl4 (150 microL/100g, 1:1 in corn oil). Pre-treated rats were given n-hexane extracts at 200 and 100 mg/kg dose 48, 24 and 2 h prior to CCl4 administration. In post-treatment groups, rats were treated with n-hexane extract at a dose of 200 and 100 mg/kg, 2, 24 and 48 h after CCl4 intoxication. Rats pre-treated with Lygodium flexuosum remarkably prevented the elevation of serum AST, ALT, LDH and liver lipid peroxides in CCl4-treated rats. Rats treated with the extract after the establishment of CCl4 induced liver injury showed significant (p < or = 0.05) protection of liver as evidenced from normal AST, ALT, LDH and MDA levels. Hepatic glutathione levels were significantly (p < or = 0.05) increased by the treatment with the extracts in both the experimental groups. Histopathological changes induced by CCl4 were also significantly (p < or = 0.05) reduced by the extract treatment in preventive and curative groups. Phytochemical studies revealed the presence of saponins, triterpenes, sterols and bitter principles in Lygodium flexuosumn-hexane extract which could be responsible for the possible hepatoprotective action.     

广东凉茶颗粒对拘束负荷诱发小鼠应激性肝损伤的保护作用

目的:研究广东凉茶颗粒对拘束负荷诱发小鼠应激性肝损伤的保护作用。方法:将实验小鼠随机分成正常对照组、拘束模型组、维生素C 250 mg.kg^-1给药组、广东凉茶颗粒500,250 mg.kg^-1给药组。18 h拘束负荷后诱发小鼠应激性肝损伤,分别用赖氏法测定小鼠血浆丙氨酸氨基转移酶(ALT)活性,硫代巴比妥酸法测定肝组织和血浆丙二醛(MDA)水平,HPLC法测定谷胱甘肽(GSH)含量,比色法测定谷胱甘肽过氧化物酶(GSH-PX)活性、谷胱甘肽S转移酶(GST)活性,G riess化学法测定一氧化氮(NO)水平和荧光酶标仪测定抗氧化能力指数(ORAC)。结果:与拘束负荷模型组相比,广东凉茶颗粒可以明显降低因拘束负荷引起的小鼠血浆ALT活性(92.75±1.91 vs 39.29±2.56,32.69±1.46)U.L^-1,保护拘束负荷诱发的应激性肝损伤。此外,广东凉茶颗粒有效地提高应激小鼠肝组织中ORAC指数、GSH含量、GSH-PX及GST活性,降低MDA和NO水平。结论:广东凉茶颗粒对拘束负荷诱发小鼠应激性肝损伤具有一定的保护作用,其作用机制可能部分来自于减少拘束负荷小鼠氧化应激水平和改善组织脂质过氧化过程。     

Ameliorative effects of pycnogenol on carbon tetrachloride-induced hepatic oxidative damage in rats

This study evaluated the putative antioxidant activity of Pycnogenol (PYC) against CCl4-induced hepatic oxidative damage in Sprague-Dawley rats. A single oral dose of CCl4 (1.25 mL/kg) produced significantly increased levels of serum aminotransferase (AST) and alanine aminotransferase (ALT) activities. In addition, increased malondialdehyde (MDA) concentration, reduced glutathione (GSH) content, and decreased catalase, superoxide dismutase (SOD) and glutathione-S-transferase (GST) activities were observed in the hepatic tissues. However, concomitant administration with PYC (10 or 20 mg/kg) significantly improved CCl4-induced hepatic injury, as evidenced by the decline of serum AST and ALT activities in a dose dependent manner. Moreover, PYC reduced MDA concentration and increased GSH levels and catalase, SOD and GST activities in hepatic tissues, indicating that concomitant administration with PYC efficiently prevent the CCl4-induced oxidative damage in rats. The free radical scavenging assay showed that PYC has a dose-dependent scavenging activity against 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals. These results indicate that PYC has an antioxidant effect against CCl4-induced hepatic oxidative damage and is useful as a hepatoprotective agent against various liver diseases induced by oxidative stress.     

穿山龙水提物对四氯化碳致急性肝损伤模型小鼠toll样受体4/髓样分化因子88通路的影响

目的 观察穿山龙水提物对四氯化碳诱导急性肝损伤模型小鼠的影响,探讨其对toll样受体4(Toll-like receptors 4,TLR4)/髓样分化因子88(Myeloid differentiation factor88,MyD88)信号通路的调控作用.方法 60只小鼠按随机数字表法分为对照组,模型组,穿山龙水提物低、中、高剂量组,每组10只.穿山龙水提物低、中、高剂量组分别灌胃50、100、200 mg/kg穿山龙水提物混悬液,对照组和模型组灌胃等体积溶剂.1次/d,连续给药7 d.末次给药后2 h,除对照组外,其余各组小鼠腹腔注射0.35%四氯化碳橄榄油溶液建立急性肝损伤模型.造模后24 h,采用Western blot检测各组肝组织TLR4、MyD88、NF-κB p65表达;采用PCR法检测各组肝组织IL-1β、TNF-α、IL-6 mRNA表达;采用ELISA法检测各组小鼠血清AST、ALT含量.结果 与模型组比较,穿山龙水提物低、中、高剂量组小鼠血清AST[(98.00±17.75)U/L、(57.49±9.66)U/L、(39.60±9.49)U/L比(113.40±9.71)U/L]、ALT[(76.00±14.73)U/L、(50.70±9.35)U/L、(35.25±9.93)U/L比(95.42±11.64)U/L]水平降低(P<0.01);穿山龙水提物高剂量组MyD88[(0.67±0.21)比(1.74±0.42)]、NF-κB p65[(0.51±0.09)比(1.76±0.31)]、TLR4[(0.97±0.25)比(2.99±0.72)]表达降低(P<0.01);穿山龙水提物中、高剂量组IL-6 mRNA[(2.22±0.25)、(1.76±0.31)比(5.20±0.60)]、IL-1βmRNA[(1.96±0.35)、(1.47±0.23)比(7.37±0.99)]、TNF-αmRNA[(2.06±0.25)、(1.34±0.33)比(2.98±0.50)]表达降低(P<0.01).结论 穿山龙水提物通过抑制TLR4/MyD88信号通路实现对四氯化碳诱导小鼠急性肝损伤的保护作用.     

Evaluation of hepatoprotective effect of Amalkadi Ghrita against carbon tetrachloride-induced hepatic damage in rats

Amalkadi Ghrita (AG), a polyherbal formulation, was evaluated for its hepatoprotective activity against carbon tetrachloride (CCl₄)-induced hepatic damage in rats. The hepatoprotective activity of AG was evaluated by measuring levels of serum marker enzymes like serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP), and acid phosphatase (ACP). The serum levels of total proteins and bilirubin were also estimated. The histological studies were also carried out to support the above parameters. Silymarin was used as standard drug. Administration of AG (100 and 300 mg/kg, p.o.) markedly prevented CCl₄-induced elevation of levels of serum GPT, GOT, ACP, ALP, and bilirubin. The decreased level of total proteins due to hepatic damage induced by CCl₄ was found to be increased in AG-treated group. The results are comparable to that of silymarin. A comparative histopathological study of liver exhibited almost normal architecture, as compared to CCl₄-treated group. Hepatoprotective effect of AG is probably due to combined action of all ingredients.