平 洁 高爱梅 徐 丹 李瑞雯 汪 晖. 吲哚-3-原醇对猪血清诱导大鼠肝纤维化的治疗作用J. 药学学报, 2011,46(8): 915-921.
引用本文: 平 洁 高爱梅 徐 丹 李瑞雯 汪 晖. 吲哚-3-原醇对猪血清诱导大鼠肝纤维化的治疗作用J. 药学学报, 2011,46(8): 915-921.
BENG Ji, Gao-Ai-Mei, Xu- Dan, Li-Rui-Wen, Hong- Hui. Therapeutic effect of indole-3-carbinol on pig serum-induced hepatic fibrosis in ratsJ. 药学学报, 2011,46(8): 915-921.
Citation: BENG Ji, Gao-Ai-Mei, Xu- Dan, Li-Rui-Wen, Hong- Hui. Therapeutic effect of indole-3-carbinol on pig serum-induced hepatic fibrosis in ratsJ. 药学学报, 2011,46(8): 915-921.

吲哚-3-原醇对猪血清诱导大鼠肝纤维化的治疗作用

Therapeutic effect of indole-3-carbinol on pig serum-induced hepatic fibrosis in rats

  • 摘要:

    研究吲哚-3-原醇 (I3C) 对猪血清诱导大鼠肝纤维化的治疗作用及其机制。腹腔注射猪血清制备大鼠肝纤维化模型, 造模成功后用I3C治疗17天。采用HEMasson三色染色法分别观察肝脏病理学和胶原含量改变; 生化比色法测定肝组织羟脯氨酸 (Hyp) 含量; 免疫组织化学法观察肝脏中α-平滑肌肌动蛋白 (α-SMA)的表达。进一步培养大鼠肝星状细胞株HSC-T6, I3C处理24 h, FITC-Annexin V/PI双重染色法检测细胞凋亡; 实时荧光定量PCR法检测细胞凋亡相关蛋白BaxBcl-2mRNA表达。结果显示, 与模型对照组比较, I3C治疗组的肝组织Hyp含量不同程度降低, 肝细胞损伤减轻, 胶原纤维沉积减少 (P < 0.01), α-SMA表达降低 (P < 0.01)细胞实验显示, I3C可明显增加HSC-T6细胞凋亡率, 升高Bax/Bcl-2mRNA表达 (P < 0.05)。以上结果说明, I3C猪血清诱导大鼠肝纤维化有一定治疗作用, 可能与其诱导活化HSC凋亡继而促进基质胶原降解有关。

     

    Abstract:

    This study is to investigate the therapeutic effect and mechanism of indole-3-carbinol (I3C) on pig serum-induced liver fibrosis of rats.  The liver fibrotic model of rats was induced by pig serum.  After models were successfully established, rats in the treatment groups were administered with I3C through intraperitoneal injection or curcumin by intragastric administration, daily for 17 days.  Hepatic hydroxyproline (Hyp) content was measured.  The liver histology and immunohistochemistry with a-smooth muscle actin (α-SMA) were assayed.  Hepatic stellate cells line, HSC-T6 was incubated with different concentrations of I3C (25, 50, and 100 mmol·L−1) for 24 h.  The effect of I3C on cell apoptosis was identified by FITC-Annexin V/PI double labeled assay.  And the mRNA expressions of Bax and Bcl-2 were measured by real time RT-PCR.  The results showed that hepatic content of Hyp decreased by I3C treatment, as compared with the fibrotic model control.  Histopathological changes, such as steatosis, necrosis, deposition of collagenous fiber reduced remarkably and the expression of α-SMA was significantly down-regulated in the I3C-treated groups (P < 0.01).  Apoptosis analysis showed that I3C significantly increased HSC-T6 apoptosis rate and the expressional ratio of Bax to Bcl-2.  The results indicated that I3C could effectively cure pig serum-induced liver fibrosis in vivo by inducing HSC apoptosis and promoting ECM degradation.

     

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