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目的观察热量限制对老化进程中小鼠骨骼肌线粒体等生物学性状的影响,探讨热量限制生物效应的分子机制。方法 13月龄C57BL/6雄性小鼠30只,按照简单随机抽样法分为自由进食组和热量限制组,每周按照自由进食组前1周平均摄食量的60%饲养热量限制小鼠。热量限制12周后,测量骨骼肌衰减指数、胫前肌等肌纤维密度及相对横截面积,透射电镜观察骨骼肌线粒体变化,Western blot检测PGC1α、AMPKα、p-AMPKα及SIRT1等的表达,并比较老年鼠与成年鼠的表达差异。结果 1与自由进食组比较,热量限制组骨骼肌衰减指数变化不明显,胫前肌等肌纤维密度显著升高(P<0.01),相对横截面积降低(P<0.01);2电镜观察显示:与自由进食组比较,热量限制组骨骼肌线粒体长度和宽度均增加(P<0.05,P<0.01),相对密度增加(P<0.01),PGC1α表达升高(P<0.05);3与自由进食组比较,热量限制组骨骼肌AMPK的磷酸化水平升高(P<0.01),同时SIRT1表达也升高(P<0.05);4与成年鼠比较,老年鼠骨骼肌AMPK磷酸化水平下降(P<0.05),SIRT1和PGC1α的表达也均下降(P<0.05)。结论热量限制能显著促进老化进程中骨骼肌线粒体的生成及活性,这一作用可能通过激活AMPK信号途径实现。
Objective To observe the effect of caloric restriction on biological characteristics of mitochondria and other mitochondria in mouse skeletal muscle during aging process and to explore the molecular mechanism of calorie restriction biological effect. Methods Thirty male C57BL / 6 13-month-old mice were divided into two groups according to the random sampling method: caloric restriction group and calorie restriction group. After 12 weeks of heat restriction, the skeletal muscle attenuation index, the muscle fiber density and relative cross-sectional area of the anterior tibial muscle were measured. The mitochondrial changes of skeletal muscle were observed by transmission electron microscopy. The expressions of PGC1α, AMPKα, p-AMPKα and SIRT1 were detected by Western blot Differences in expression between old and adult rats. Results 1 Compared with the free-fed group, there was no significant change in the skeletal muscle atherosclerosis index (P <0.01) and the relative cross-sectional area (P <0.01) (P <0.05, P <0.01), the relative density increased (P <0.01) and PGC1α expression increased (P <0.05). Compared with the free feeding group, the mitochondria length and width increased Compared with the control group, AMPK phosphorylation in skeletal muscle increased (P <0.01) and SIRT1 expression increased (P <0.05). 4 Compared with adult mice, AMPK phosphorylation in skeletal muscle decreased <0.05), the expression of SIRT1 and PGC1α also decreased (P <0.05). Conclusion Caloric restriction can significantly promote the generation and activity of skeletal muscle mitochondria during the aging process, which may be achieved through the activation of AMPK signaling pathway.