【摘要】：目的建立慢性寒冷暴露模型,觀察冷應(yīng)激對線粒體數(shù)量、形態(tài)學(xué)調(diào)控蛋白及生物合成的影響并對其機制進行初步探討。方法選取8周齡健康雄性C57BL/6J小鼠40只,隨機分為對照組和寒冷組,每組各20只。寒冷組于-4~0℃環(huán)境中飼養(yǎng)4周建立慢性寒冷暴露模型。采用Mito Tracker在體標記小腦皮質(zhì)顆粒細胞線粒體的方法統(tǒng)計線粒體的數(shù)量,同時應(yīng)用免疫熒光染色法和Western blotting技術(shù),檢測線粒體分裂、融合蛋白及轉(zhuǎn)錄輔激活因子過氧化物酶體增殖活化受體γ輔助活化因子1α(PGC-1α)的表達情況。結(jié)果與對照組相比,寒冷組線粒體數(shù)量增多(P0.01),線粒體分裂、融合蛋白及轉(zhuǎn)錄輔激活因子PGC-1α表達均顯著增多(P0.01)。結(jié)論慢性寒冷暴露可能通過誘導(dǎo)PGC-1α的高表達增強線粒體生物合成,增加線粒體數(shù)量;活化的PGC-1α協(xié)同冷應(yīng)激促進線粒體形態(tài)學(xué)調(diào)控蛋白表達,構(gòu)建新的分裂和融合的動態(tài)平衡,為機體適應(yīng)低溫環(huán)境提供高效率的產(chǎn)能機制。
[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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