Effects of silver needle-thermal conduction therapy on skeletal muscle mitochondria and silent information regulator homolog 3 expression in a rat model of myofascial pain syndrome

doi:10.12307/2024.300

Abstract

Abstract: BACKGROUND: Clinical studies have found good analgesic effects of silver needle-thermal conduction therapy in patients with myofascial pain syndrome, but the exact mechanism remains unclear.
OBJECTIVE: To observe the effect of silver needle-thermal conduction therapy on silent information regulator homolog 3 (SIRT3) changes and mitochondrial ultrastructure in a rat model of myofascial pain syndrome.
METHODS: Twenty rats were randomly selected from 26 Sprague-Dawley rats and were subjected to percussion combined with motor fatigue for replicating the rat model of myofascial pain syndrome. Sixteen rats that were successfully modeled were randomly divided into model group and silver needle-thermal conduction therapy group (treatment group), with eight rats in each group. The remaining rats were used as controls (normal group). The treatment group was treated with silver needle-thermal conduction therapy. Mechanical withdrawal threshold and thermal withdrawal latency of rats were measured at 1 day before modeling, 1 day after modeling and 14 days after treatment. Electromyographic activities of the right medial femoral muscle were measured at 14 days after treatment. The right medial femoral muscle tissue was taken for hematoxylin-eosin staining to observe the local morphology and for transmission electron microscopy to observe the mitochondrial ultrastructure. Western blot assay was performed to detect SIRT3 expression.
RESULTS AND CONCLUSION: Pain threshold: The mechanical withdrawal threshold and thermal withdrawal latency of the model and treatment groups were significantly decreased compared with those in the normal group and before modeling (P < 0.01). After treatment, the mechanical withdrawal threshold and thermal withdrawal latency of rats were significantly higher in the treatment group compared with the model group (P < 0.01). Electromyography: The rats in the model group showed spontaneous electrical activity in the right medial femur, while the rats in the treatment group showed reduced spontaneous electrical activity, longer time frame (P < 0.01) and lower wave amplitude (P < 0.05) compared with the model group. Hematoxylin-eosin staining: In the normal group, rat muscle fibers arranged closely and regularly. In the model group, the muscle fibers of rats were atrophied, degenerated, and disordered in arrangement. In the treatment group, rat muscle structure disorder improved. Mitochondrial microstructure: Under the transmission electron microscope, mitochondrial structure in the normal group was normal; mitochondrial swelling with broken or disappeared cristae appeared in the model group; mitochondrial swelling in the treatment group was obviously relieved or tended to be normal. SIRT3 expression: SIRT3 expression was significantly downregulated in the model group compared with the normal group, but was significantly upregulated in the treatment group compared with the model group (P < 0.05). To conclude, abnormalities in local muscle mitochondria and downregulation of SIRT3 expression suggest the presence of impaired energy metabolism in the rat model of myofascial pain syndrome. Mitochondrial changes recover and are close to normal after the silver needle-thermal conduction therapy, and the expression of SIRT3 is also upregulated close to the normal group, indicating the silver needle-thermal conduction therapy may play a therapeutic role by promoting mitochondrial repair and improving energy metabolism disorder.

Key words: myofascial pain syndrome, silver needle-thermal conduction therapy, muscle mitochondria, SIRT3, myofascial trigger point

CLC Number:

Wang Yue, Zhang Yuhan, Wang Jiayi, Huang Yuanxin, Wo Chunxin, Wang Caixia, Zhou Peiran, Wang Lin. Effects of silver needle-thermal conduction therapy on skeletal muscle mitochondria and silent information regulator homolog 3 expression in a rat model of myofascial pain syndrome[J]. Chinese Journal of Tissue Engineering Research, 2024, 28(14): 2202-2208.

Figures/Tables 6

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