花色苷对肝纤维化模型小鼠的干预作用

Effect of anthocyanin on the CCl_4 induced hepatic fibrosis in rat model

目的探讨花色苷对CCl_4导致肝纤维化模型小鼠的改善作用,并初步探讨其抗纤维化的作用机制。方法将30只Balb/c小鼠随机分为空白对照组、CCl_4组和CCl_4+花色苷组。空白对照组给予生理盐水灌胃和玉米油腹腔注射,CCl_4组给予生理盐水灌胃和溶于玉米油的10%CCl_4腹腔注射,花色苷组给予10μg/g的花色苷灌胃和溶于玉米油的10%CCl_4腹腔注射。结合常规HE、苦味酸-天狼猩红染色评价肝组织炎症及纤维化程度,Western blot和q-PCR检测肝脏α-平滑肌肌动蛋白(α-SMA)、Ⅰ型胶原蛋白(COL1A1)以及转化生长因子-β1(TGF-β1)的表达水平,并通过激光共聚焦检测肝星状细胞自噬水平。结果花色苷干预组与CCl_4组相比纤维化指标检测均有降低且差异具有统计学意义(P<0.05),肝星状细胞的活化与自噬水平受到抑制。结论花色苷能够改善CCl_4所致肝纤维化水平,可能与降低肝星状细胞的自噬水平有关。

Objective To observe the intervention effect and mechanism of anthocyanin on the CCL induced hepatic fibrosis in rat models. Methods 30 mice were randomly divided into normal control group （group A）, CC14 group （group B ）, CCI,＋ anthocyanin group （group C） , and there were 10 mice in each group. These groups were separately established by intraperitoneal injection of normal saline, carbon tetrachloride （CC14） and CCL, respectively. Group A and B were intragastric administrated with normal saline for group A and B, and group C with anthocyanin. The effect on the fibrosis degrees of hepatic tissues was evaluated by routine pathological HE and Sirius Red Staining. The expression levels of c^- SMA, COL1A1 and TGF-131 were detected using western blot and q-PCR, and the autophagy level of hepatic stellate cell was evaluated through the laser confocal microscope. Results Compared with CC14 group, the fibrosis and autophagy indexes of group C were both significantly lower （P〈0.05）. Conclusion Anthocyanin could reduce the liver fibrosis level induced by CClg, which might due to the suppression of the activation of hepatic stellate cell and the formation of autophagosome.