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首页> 外文期刊>Acta Pharmacologica Sinica >Rhein inhibits liver fibrosis induced by carbon tetrachloride in rats
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Rhein inhibits liver fibrosis induced by carbon tetrachloride in rats

机译:大黄酸抑制大鼠四氯化碳引起的肝纤维化

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AIM: To investigate the effect of rhein on liver fibrosis induced by the exposure of carbon tetrachloride (CCl_4)/ ethanol in rats. METHODS: Male Wistar rats were divided into four study groups (n=10 each group): healthy controls, CCl_4/ethanol-injured rats left untreated, and CCl_4/ethanol-injured rats treated with rhein of low-dose (25 mg·kg~(-1)) and high-dose (100 mg·kg~(-1)). Rhein was given once a day since rat received CCl_4/ethanol injury. After administration of rhein for 6 weeks rats were killed. The following parameters were determined: the activity of alanine aminotransferase (ALT), hyalauronic acid (HA) and procollagen type Ⅲ (PC-Ⅲ) concentrations in serum, liver malondialdehyde (MDA) level, the degree of liver fibrosis, and the expression of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) in liver tissue. RESULTS: The treatment of rhein markedly reduced the ALT activity, HA and PC-Ⅲ concentrations, and liver MDA level in CCl_4/ethanol-injured rats (P<0.01). It also improved significantly histological changes of fibrosis and decreased the expression of α-SMA and TGF-β1 in liver of these rats (P<0.05 or P<0.01). CONCLUSION: Rhein has protective effect on liver injury and can inhibit liver fibrosis induced by CCl_4/ethanol in rats. The mechanisms possibly contribute to its action of antioxidant and anti-inflammatory activity, also associated with its effect of inhibiting TGF-β1 and suppressing the activation of hepatic stellate cells.
机译:目的:研究大黄酸对四氯化碳(CCl_4)/乙醇暴露引起的大鼠肝纤维化的影响。方法:雄性Wistar大鼠分为四个研究组(每组n = 10):健康对照组,未经治疗的CCl_4 /乙醇损伤大鼠和用低剂量大黄酸(25 mg·kg)治疗的CCl_4 /乙醇损伤大鼠。 〜(-1))和大剂量(100 mg·kg〜(-1))。自大鼠受到CCl_4 /乙醇损伤后,每天给予大黄酸一次。施用大黄酸6周后,处死大鼠。确定以下参数:血清中丙氨酸氨基转移酶(ALT)活性,透明质酸(HA)和Ⅲ型胶原原(PC-Ⅲ)浓度,肝丙二醛(MDA)水平,肝纤维化程度以及肝纤维化的表达肝组织中的α平滑肌肌动蛋白(α-SMA)和转化生长因子β1(TGF-β1)。结果:大黄酸处理可显着降低CCl_4 /乙醇损伤大鼠的ALT活性,HA和PC-Ⅲ浓度以及肝脏MDA水平(P <0.01)。它还显着改善了这些大鼠肝脏的纤维化组织学变化,并降低了α-SMA和TGF-β1的表达(P <0.05或P <0.01)。结论大黄酸对大鼠肝损伤具有保护作用,并能抑制CCl_4 /乙醇诱导的肝纤维化。该机制可能有助于其抗氧化和抗炎活性,还与抑制TGF-β1和抑制肝星状细胞活化有关。

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