| 徐渴阳,苏晓倩,包剑锋.基于细胞自噬探讨气虚血瘀型肝纤维化大鼠的分子机制[J].浙江中西医结合杂志,2019,29(4): |
| 基于细胞自噬探讨气虚血瘀型肝纤维化大鼠的分子机制 |
| The molecular mechanism of liver fibrosis in rats with qi deficiency and blood stasis based on autophagy |
| 投稿时间：2018-10-16 修订日期：2018-11-09 |
| DOI： |
| 中文关键词: 细胞自噬 气虚血瘀 肝纤维化 |
| 英文关键词:autophagy qi deficiency and blood stasis liver fibrosis LC3II P62 |
| 基金项目:从Nrf2-Keap1-Are信号通路探讨细胞自噬对气虚血瘀型肝纤维化的作用机制 |
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| 中文摘要: |
| 摘要 目的 探讨气虚血瘀肝纤维化大鼠细胞自噬基因LC3II和p62的mRNA、蛋白表达水平及扶正化瘀胶囊的干预效果。方法40只SD大鼠根据随机数字表法分正常组、肝纤维化组、气虚血瘀肝纤维化组、扶正化瘀治疗组，处死后予以天狼星红染色，并分别测定肝重、肝湿重。采用qPCR、Western blot测定LC3II、p62 mRNA和蛋白的表达水平。结果 治疗组体重(375.80±24.36)及肝湿重(11.31±1.13)，分别高于气虚血瘀肝纤维化组(356.10±20.45; 10.34±1.13，p＜0.05）；天狼星红染色提示，气虚血瘀肝纤维化组肝纤维最重，治疗后显著改善；Ishak评分在气虚血瘀肝纤维化组（20.001.60）最高，扶正化瘀治疗组（12.90±1.90）显著下降（p＜0.05）。LC3II mRNA（1.44± 0.01）及蛋白（3.01± 0.57）表达在气虚血瘀肝纤维化组最高，治疗组LC3II mRNA（1.20±0.01）、及蛋白(1.12± 0.01）均显著下降（p＜0.05）；而P62 mRNA（0.95±0.05）及蛋白（0.19±0.12）在气虚血瘀肝纤维化组最低，扶正化瘀治疗组P62 mRNA（2.04±0.30）及蛋白（0.67±0.32）显著升高（p＜0.05）。结论 气虚血瘀型肝纤维化大鼠较单纯肝纤维化大鼠LC3II表达明显增加，而自噬底物p62消耗明显，并与纤维化严重程度呈正相关，且通过扶正化瘀胶囊干预可以显著抑制LC3II/ p62通路。 |
| 英文摘要: |
| ABSTRACT Objective To investigate the levels of mRNA, protein expression and the effect of Fuzhenghuayu capsule on the autophagy gene LC3II and p62 of liver fibrotic cells in rats with qi deficiency and blood stasis. Methods Forty SD rats were divided into normal group, liver fibrosis group, qi deficiency and blood stasis group and treatment group according to the random number table method. The expression levels of LC3II, p62 mRNA and protein were measured by qPCR and Western blot. Results Body weight (375.80±24.36) and liver wetting weight (11.31±1.13) were higher in the treatment group than those in the treatment group (356.10±20.45，10.34±1.13, p < 0.05). Sirius red staining indicated that liver fibers were the heaviest in the group of qi deficiency and blood stasis, which was significantly improved after treatment. Ishak scores were highest in the qi-deficiency and blood-stasis group (20.00±1.60) and significantly decreased in the treatment group (12.90±1.90) (p < 0.05). LC3II mRNA (1.44±0.01) and protein (3.01±0.57) were highest in the qi-deficiency and blood-stasis group, and LC3II mRNA (1.20±0.01) in the treatment group. And protein (1.12±0.01) decreased significantly (p < 0.05). P62 mRNA (0.95±0.05) and protein (0.19±0.12) were the lowest in the qi-deficiency and blood-stasis group, while P62 mRNA (2.04±0.30) and protein (0.67 + 0.32) were significantly increased in the treatment group (p < 0.05). Conclusion The expression of LC3II in rats with qi-deficiency and blood-stasis liver fibrosis was significantly increased, while the consumption of autophagy substrate p62 was significantly increased, which was positively correlated with the severity of fibrosis, and LC3II/ p62 pathway was significantly inhibited by the intervention of fuzheng huayu capsule. |
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