Effect of acupuncture on mitophagy of skeletal muscle in rats with exercise-induced skeletal muscle damage

AIM: The effect of acupuncture on mitophagy-related protein expression in skeletal muscle of rats after heavy-load exercise was investigated to explore the role of acupuncture in the repairment of exercise-induced skeletal muscle damage. METHODS: Male adult Sprague-Dawley rats (n=128) were randomly divided into 4 groups:control (C, n=8) group, exercise (E, n=40) group, acupuncture (A, n=40) group, and exercise and acupuncture (EA, n=40) group. The rats in E group and EA group performed an eccentric exercise, and the rats in A group and EA group immediately after exercise received acupuncture treatment. The rats in the latter 3 groups were further divided into 0 h, 12 h, 24 h, 48 h and 72 h sub-groups (n=8), and soleus muscle was collected at each time point. The transmission electron microscopy was used to observe the ultrastructural changes of the mitochondria in skeletal muscle. The content of citrate synthase (CS) was measured by ELISA. The protein expression of skeletal muscle PTEN-induced putative kinase 1 (PINK1), parkin and microtubule-associated protein 1 light chain 3 (LC3) was determined by Western blot. RESULTS: After the heavy-load exercise, the mitochondria swelled and accumulated under cell membrane. The number of mitophagosomes was increased, and the content of CS was significantly decreased (P<0.05). The expression of PINK1, parkin and LC3 was significantly elevated (P<0.05). However, the acupuncture intervention after exercise promoted the recovery of mitochondrial ultrastructure, attenuated mitophagolysosome formation, maintained CS content and down-regulated the expression of PINK1, parkin and LC3 (P<0.05). CONCLUSION: Heavy-load exercise causes the damages of mitochondrial structure and function in the skeletal muscle and activates PINK1/parkin pathway to induce excessive occurrence of mitophagy. Acupuncture intervention after exercise is able to alleviate the damage of mitochondria in the skeletal muscle through decreasing the expression of mitochondrial outer membrane protein PINK1, reducing the recruitment of downstream cytoplasmic protein parkin, thereby affecting the combination of LC3 and mitochondria to inhibit the overactivation of mitophagy.