慢性寒冷暴露与线粒体数量改变

发布时间：2018-07-22 13:26

【摘要】：目的建立慢性寒冷暴露模型,观察冷应激对线粒体数量、形态学调控蛋白及生物合成的影响并对其机制进行初步探讨。方法选取8周龄健康雄性C57BL/6J小鼠40只,随机分为对照组和寒冷组,每组各20只。寒冷组于-4~0℃环境中饲养4周建立慢性寒冷暴露模型。采用Mito Tracker在体标记小脑皮质颗粒细胞线粒体的方法统计线粒体的数量,同时应用免疫荧光染色法和Western blotting技术,检测线粒体分裂、融合蛋白及转录辅激活因子过氧化物酶体增殖活化受体γ辅助活化因子1α(PGC-1α)的表达情况。结果与对照组相比,寒冷组线粒体数量增多(P0.01),线粒体分裂、融合蛋白及转录辅激活因子PGC-1α表达均显著增多(P0.01)。结论慢性寒冷暴露可能通过诱导PGC-1α的高表达增强线粒体生物合成,增加线粒体数量;活化的PGC-1α协同冷应激促进线粒体形态学调控蛋白表达,构建新的分裂和融合的动态平衡,为机体适应低温环境提供高效率的产能机制。
[Abstract]:Objective to establish a model of chronic cold exposure and to investigate the effects of cold stress on the number of mitochondria, morphological regulatory proteins and biosynthesis. Methods Forty healthy 8-week-old C57BL / 6J mice were randomly divided into control group and cold group with 20 in each group. The cold group was fed with 4 Zhou Jianli chronic cold exposure model at -4 鈩，

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