Guo Mei-Zi, Li Xiao-Sheng, Xu Hai-Rong, Mei Zhe-Chuan, Shen Wei, Ye Xiu-Feng
Department of Gastroenterology, Second Affiliated Hospital, Chongqing 400010, China.
Acta Pharmacol Sin. 2002 Aug;23(8):739-44.
To investigate the effect of rhein on liver fibrosis induced by the exposure of carbon tetrachloride (CCl4)/ethanol in rats.
Male Wistar rats were divided into four study groups (n=10 each group): healthy controls, CCl4/ethanol-injured rats left untreated, and CCl4/ethanol-injured rats treated with rhein of low-dose (25 mg/kg) and high-dose (100 mg/kg). Rhein was given once a day since rat received CCl4/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 alpha-smooth muscle actin (alpha-SMA) and transforming growth factor-beta1 (TGF-beta1) in liver tissue.
The treatment of rhein markedly reduced the ALT activity, HA and PC-III concentrations, and liver MDA level in CCl4/ethanol-injured rats (P<0.01). It also improved significantly histological changes of fibrosis and decreased the expression of alpha-SMA and TGF-beta1 in liver of these rats (P<0.05 or P<0.01).
Rhein has protective effect on liver injury and can inhibit liver fibrosis induced by CCl4/ethanol in rats. The mechanisms possibly contribute to its action of antioxidant and anti-inflammatory activity, also associated with its effect of inhibiting TGF-beta1 and suppressing the activation of hepatic stellate cells.
研究大黄酸对四氯化碳（CCl4）/乙醇诱导的大鼠肝纤维化的影响。
雄性Wistar大鼠分为四个研究组（每组n = 10）：健康对照组、未治疗的CCl4/乙醇损伤大鼠，以及用低剂量（25 mg/kg）和高剂量（100 mg/kg）大黄酸治疗的CCl4/乙醇损伤大鼠。自大鼠受到CCl4/乙醇损伤后，每天给予一次大黄酸。给予大黄酸6周后处死大鼠。测定以下参数：血清中丙氨酸转氨酶（ALT）活性、透明质酸（HA）和III型前胶原（PC-III）浓度、肝脏丙二醛（MDA）水平、肝纤维化程度，以及肝组织中α-平滑肌肌动蛋白（α-SMA）和转化生长因子-β1（TGF-β1）的表达。
大黄酸治疗显著降低了CCl4/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）。它还显著改善了纤维化的组织学变化，并降低了这些大鼠肝脏中α-SMA和TGF-β1的表达（P < 0.05或P < 0.01）。
大黄酸对肝损伤具有保护作用，可抑制CCl4/乙醇诱导的大鼠肝纤维化。其机制可能与其抗氧化和抗炎活性作用有关，也与其抑制TGF-β1和抑制肝星状细胞活化的作用有关。
