有氧耐力运动引起的自噬在骨骼肌建成中的作用
发布时间：2018-08-03 10:08
【摘要】：目的：通过建立一个小鼠有氧运动模型，探讨自噬在运动引起的肌肉建成中的作用及其分子机制。 方法：建立雌性小鼠转轮运动模型：6米/分钟，15分钟/次，，3次/天（8:00，14:00和20:00），5天/周，共8周。采用自噬激活剂海藻糖（1％水溶液，自由饮用）为阳性对照，自噬抑制剂氯喹（10mg/kg体重，腹腔注射），为阴性对照。Western blot检测运动对自噬蛋白P62，LC3和Cathepsin L，抗凋亡蛋白Bcl-2和前凋亡蛋白Bnip3的影响，TUNEL法检测骨骼肌细胞凋亡的变化情况，HE染色和透射电子显微镜检测骨骼肌，线粒体和自噬体的形态变化。 结果：运动显著降低小鼠的体重和腹腔脂肪量，提高自由基的清除能力，促进自噬体的形成，增加蛋白LC3-II，Cathepsin L，BCL-2的表达和减少P62和Bnip3的蛋白表达。同时，运动后小鼠骨骼肌中线粒体形态和细胞凋亡情况得到明显改善。运动引起线粒体中细胞色素C的增加，细胞质中细胞色素C的下降，阻止细胞色素C从线粒体释放至细胞质。自噬诱导剂海藻糖激活骨骼肌自噬，对骨骼肌表现出保护作用；抑制剂氯喹阻断自噬流量，破坏肌纤维和线粒体形态。长期有规律运动没有进一步增强海藻糖的作用，但可以部分恢复氯喹对小鼠骨骼肌的有害影响。 结论：长期有规律的运动通过维持骨骼肌细胞的自噬在一个较高的生理水平，保护线粒体的形态和功能，从而增强了骨骼肌的建成。
[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.
【学位授予单位】：苏州大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R87
本文编号：2161410
[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.
【学位授予单位】：苏州大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R87
【参考文献】
相关期刊论文 前1条
1 卢健,陈彩珍,许永刚,赖荣兴;运动训练对小鼠心肌线粒体能量转换功能增龄性改变的影响[J];中国应用生理学杂志;2001年01期
本文编号：2161410
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