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中文摘要：
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（P〈0.01）,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（P〈0.01）。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。
英文摘要：
Objective To investigate how chronic cold exposure influences mitochondrial quantity in cortical neurons and to explore its mechanism with a mice model. Methods Forty male mice of the age of 8 weeks were randomly divided into the control and cold exposure groups. Cold exposure group as an animal model was fed at temperature from - 4℃ to 0℃ for 4 weeks, and the control group lived in the standard laboratory situation. Mitochondria of granular cells in cerebellar cortex in vivo were labeled with MitoTracker, and the expression of mitochondrial fission and fusion proteins and peroxisome proliferators-activated receptor-γ eoactivator-1α （PGC-1α） were analyzed with immunocytochemistry and Western blotting. Results Compared with the control group, the number of mitochondria increased （P 〈 0. 01 ） and the expression of mitoehondrial fission, fusion protein and PGC-1α significantly increased （ P 〈 0.01 ） in the cold exposure group. Conclusion Chronic cold exposure may enhance mitochondrial biosynthesis to increase the quantity of mitochondria by activating PGC-1α, while activated PGC-1α can induce the expression of mitochondrial morphology regulatory proteins under cold stress. The new balance of fission and fusion of mitochondria is established at cold environment, leading to adapt to cold situation.
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