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Preventive Effects of Electrical Stimulation on Cachexia‐Induced Muscle Mitochondrial Dysfunction

Cachexia is a complex metabolic syndrome associated with underlying chronic diseases. In the cachectic muscle, mitochondrial function is damaged by pro‐inflammatory cytokines, e.g., tumor necrosis factor alpha (TNF‐α). It has been shown that electrical stimulation (ES) prevents mitochondrial dysfunction in skeletal muscle under many conditions. Therefore, the aim of this study was to evaluate the effect of electrical stimulation on cachexia‐induced mitochondrial dysfunction in skeletal muscle. ICR mice (n = 15) were randomly divided into 3 groups; lipopolysaccharide (LPS) injection, and LPS injection plus ES, and age‐matched control group. Cachexia was induced by LPS (10 mg/g body weight, i.p.) for 4 days. ES was conducted twice a day during injected period. LPS injection resulted in increase of the expression of TNF‐α, and decrease of body weight and muscle wet weight. Succinate dehydrogenase (SDH) activity and citrate synthase (CS) activity, the indicators of mitochondrial function, were decreased in the cachectic muscle. On the other hand, the intervention of ES prevented the decrease of muscle wet weight, SDH activity, and CS activity. In addition, it has been shown that p38 mitogen‐activated protein kinase (p38 MAPK) is activated by TNF‐α, and decrease the expression of PPAR gamma coactivator 1‐alhpa (PGC‐1α) which is the mitochondrial biogenesis factor in cachectic muscle. In this study, cachexia‐associated changes in PGC‐1α was prevented by ES via p38 MAPK down regulation. These results suggest that electrical stimulation prevents mitochondrial dysfunction in skeletal muscle induced by pro‐inflammatory cytokines which express in cachexia.