Kallistatin通过Akt-eNOS信号通路对肝星状细胞氧化损伤的保护作用

发布时间：2018-04-19 11:31

本文选题：组织激肽释放酶结合蛋白 + 肝星状细胞　；参考：《药学学报》2017年09期

【摘要】：为揭示kallistatin对肝星状细胞氧化损伤的保护作用及相关分子机制,本文以过氧化氢和铁过载为氧化模型,以大鼠原代肝星状细胞及完全活化的人肝星状细胞系LX-2为对象,研究了kallistatin在对肝星状细胞活力、超氧化物、NADPH和Akt、e NOS等分子的影响。实验结果显示,kallistatin既能避免肝星状细胞受氧化损伤,还能修复氧化应激造成的细胞损伤;其主要机制为kallistatin能清除细胞内的超氧化物、降低细胞内NADPH活力;另外,kallistatin还能激活Akt和e NOS等分子发挥抗氧化作用。本研究为加速肝纤维化药物新靶点开发提供了理论依据。
[Abstract]:In order to reveal the protective effect of kallistatin on oxidative damage of hepatic stellate cells and its related molecular mechanisms, hydrogen peroxide and iron overload were used as oxidation models, and rat primary hepatic stellate cells and fully activated human hepatic stellate cell line LX-2 were used as subjects.The effects of kallistatin on the activity of hepatic stellate cells, superoxide NADPH and NOS were studied.The results showed that kallistatin could not only avoid oxidative damage of hepatic stellate cells, but also repair the oxidative stress, and its main mechanism was that kallistatin could scavenge the superoxide and decrease the activity of NADPH in the cells.In addition, kallistatin can also activate Akt, e NOS and other molecules to play an antioxidant role.This study provides a theoretical basis for accelerating the development of new drug targets for liver fibrosis.
【作者单位】：泉州师范学院化工与材料学院;华侨大学分子药物学研究院;
【基金】：国家自然科学基金资助项目(81502687,81371669) 福建省自然科学基金资助项目(2017J01548) 泉州市科技计划项目(2016Z070,2016N006) 华侨大学中青年教师科技创新资助计划(ZQN-PY319)
【分类号】：R575.2

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