【摘要】：目的：通過建立一個(gè)小鼠有氧運(yùn)動(dòng)模型，探討自噬在運(yùn)動(dòng)引起的肌肉建成中的作用及其分子機(jī)制。 方法：建立雌性小鼠轉(zhuǎn)輪運(yùn)動(dòng)模型：6米/分鐘，15分鐘/次，，3次/天（8:00，14:00和20:00），5天/周，共8周。采用自噬激活劑海藻糖（1％水溶液，自由飲用）為陽性對照，自噬抑制劑氯喹（10mg/kg體重，腹腔注射），為陰性對照。Western blot檢測運(yùn)動(dòng)對自噬蛋白P62，LC3和Cathepsin L，抗凋亡蛋白Bcl-2和前凋亡蛋白Bnip3的影響，TUNEL法檢測骨骼肌細(xì)胞凋亡的變化情況，HE染色和透射電子顯微鏡檢測骨骼肌，線粒體和自噬體的形態(tài)變化。 結(jié)果：運(yùn)動(dòng)顯著降低小鼠的體重和腹腔脂肪量，提高自由基的清除能力，促進(jìn)自噬體的形成，增加蛋白LC3-II，Cathepsin L，BCL-2的表達(dá)和減少P62和Bnip3的蛋白表達(dá)。同時(shí)，運(yùn)動(dòng)后小鼠骨骼肌中線粒體形態(tài)和細(xì)胞凋亡情況得到明顯改善。運(yùn)動(dòng)引起線粒體中細(xì)胞色素C的增加，細(xì)胞質(zhì)中細(xì)胞色素C的下降，阻止細(xì)胞色素C從線粒體釋放至細(xì)胞質(zhì)。自噬誘導(dǎo)劑海藻糖激活骨骼肌自噬，對骨骼肌表現(xiàn)出保護(hù)作用；抑制劑氯喹阻斷自噬流量，破壞肌纖維和線粒體形態(tài)。長期有規(guī)律運(yùn)動(dòng)沒有進(jìn)一步增強(qiáng)海藻糖的作用，但可以部分恢復(fù)氯喹對小鼠骨骼肌的有害影響。 結(jié)論：長期有規(guī)律的運(yùn)動(dòng)通過維持骨骼肌細(xì)胞的自噬在一個(gè)較高的生理水平，保護(hù)線粒體的形態(tài)和功能，從而增強(qiáng)了骨骼肌的建成。
[Abstract]:Aim: to investigate the role of autophagy in muscle formation induced by exercise and its molecular mechanism by establishing an aerobic exercise model in mice. Methods: a female mouse model of rotating wheel movement was established, which consisted of 15 minutes / minute / day (8: 00: 1400 and 20:00) for 5 days / week for 8 weeks. Autophagy activator trehalose (1% aqueous solution, free drinking) was used as positive control, and autophagy inhibitor chloroquine (10mg/kg body weight) was used as positive control. The effects of exercise on autophagy protein P62C3 and Cathepsin L, anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bnip3 were detected by HE staining and transmission electron microscopy (TEM). Morphological changes of mitochondria and autophagy. Results: exercise significantly decreased the body weight and abdominal fat, increased the free radical scavenging ability, promoted the formation of autophagy, increased the expression of protein LC3-III, Cathepsin LnBCL-2, and reduced the protein expression of P62 and Bnip3. At the same time, the morphology and apoptosis of mitochondria in skeletal muscle of mice were obviously improved after exercise. Exercise induced the increase of cytochrome C in mitochondria and the decrease of cytochrome C in cytoplasm, which prevented the release of cytochrome C from mitochondria to cytoplasm. Autophagy inducer trehalose activates skeletal muscle autophagy and protects skeletal muscle. Chloroquine, an inhibitor, blocks autophagy flow and destroys muscle fiber and mitochondria morphology. Long-term regular exercise did not further enhance the effect of trehalose, but partially recovered the harmful effect of chloroquine on skeletal muscle of mice. Conclusion: Long-term regular exercise enhances skeletal muscle formation by maintaining autophagy of skeletal muscle cells at a higher physiological level and protecting the morphology and function of mitochondria.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R87

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相關(guān)期刊論文 前1條

1 盧健,陳彩珍,許永剛,賴榮興;運(yùn)動(dòng)訓(xùn)練對小鼠心肌線粒體能量轉(zhuǎn)換功能增齡性改變的影響[J];中國應(yīng)用生理學(xué)雜志;2001年01期

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