ABSTRACT
OBJECTIVE: To observe the effects of electroacupuncture (EA) at "Zusanli" (ST36) on the ultrastructure and mitochondrial dynamics of skeletal muscle tissue in spleen qi deficiency rats, so as to explore the partial action mechanism of EA at ST36 for spleen deficiency syndrome. METHODS: Twenty-four male SD rats were randomly divided into 4 groups: normal group, model group, ST36 group and non-acupoint group (n＝6 in each group). The model of spleen qi deficiency syndrome was established by improper diet and exhaustive swimming. EA (2 Hz/15 Hz, 0.5 mA) was applied to bilateral ST36 in the ST36 group and non-acupoint in the non-acupoint group for 20 min, once daily for 7 days. The colorimetric method was used to detect the ATP content in skeletal muscle tissue. The ultrastructure changes of skeletal muscle tissue were observed by transmission electron microscopy. The expression levels of optic atrophy 1 (Opa1) and dynamin-related protein 1 (Drp1) mRNA and proteins in the skeletal muscle tissue were determined by fluorescence quantitative real-time PCR and Western blot, respectively. RESULTS: The ATP content in skeletal muscle tissue of model group was significantly lower than that in the normal group (P<0.05), while significantly higher in the ST36 group than that in the model group and non-acupoint group (P<0.05). Transmission electron microscopy showed that a large number of muscle fibers that were ruptured, damaged, and disorganized; moreover, many vacuoles with different sizes, and abnormally shaped or swollen mitochondria were observed in the model group. ST36 treatment improved the disor-dered fiber arrangement, and reduced the population of damaged mitochondria; thus, fused and elongated mitochondria were readily observed. Compared with the model group, there were no obvious improvements in the non-acupoint group. Compared with the normal group, the expression levels of Opa1 and Drp1 mRNAs and proteins in the skeletal muscle tissue were significantly lower in the model group (P<0.05). After the treatment, the expression levels of Opa1 and Drp1 mRNAs and proteins were up-regulated in the ST36 group (P<0.05), and the expression of Drp1 protein was up-regulated in the non-acupoint group (P<0.05)．. CONCLUSION: EA at ST36 can correct the imbalance of mitochondrial fission and fusion in skeletal muscle of rats with spleen qi deficiency, thereby improving the damage of mitochondrial structure and function, and leading to an increase of energy metabolism.