Electroacupuncture alleviates multifidus muscle injury by modulating mitochondrial function and Ca2+ uptake

Multifidus muscles maintain the stability of the lumbar spine and play a crucial role in the pathogenesis of nonspecific lower back pain. Previous studies have shown that electroacupuncture (EA) can relieve the symptoms of low back pain and reduce injury to the lumbar multifidus muscles. In this study, a rat model of lumbar multifidus muscle injury was established by 0.05% bupivacaine injection and subsequently treated with EA at bilateral "Weizhong" (BL40) acupoints. Disruption of the function and structure of multifidus muscles, increased cytosolic Ca2+ in multifidus myocytes, and reduced mitochondrial fission and ATP production were observed in the model group. Additionally, increased expression of the mitochondrial calcium uniporter (MCU) promoted mitochondrial reuptake of Ca2+ , reversing the excessive increase in cytoplasmic Ca2+ . However, the excessive increase in MCU not only aggravated the increased cytoplasmic Ca2+ but also decreased the expression of the mitochondrial division proteins dynamin-related protein 1 (Drp1) and mitochondrial fission factor (MFF). EA inhibited the overexpression of MCU, promoted mitochondrial reuptake of Ca2+ , and reversed cytosolic Ca2+ overload. Furthermore, EA regulated the expression of the mitochondrial fission proteins Drp1 and MFF and promoted the production of ATP, helping the recovery of mitochondrial function after multifidus injury. Therefore, EA can protect against bupivacaine-induced mitochondrial dysfunction, possibly by attenuating MCU overexpression in the inner mitochondrial membrane and reducing Ca2+ overloading in muscle cells, thereby protecting mitochondrial function and maintaining the normal energy demand of muscle cells.腰多裂肌维持腰椎的稳定性，在非特异性下腰痛发病中发挥重要作用。前期研究表明电针(EA)能够缓解腰痛症状，减轻腰多裂肌损伤。本研究通过0.05%布比卡因注射制备腰多裂肌损伤大鼠模型，并在“委中”(BL40)穴进行EA干预。结果显示，模型组多裂肌的结构和功能异常，肌细胞胞浆Ca2+ 增加，线粒体分裂和ATP的产生能力降低。本研究还发现一定程度的线粒体钙单向转运体(MCU)增加，可促使线粒体重摄取Ca2+ ,从而逆转胞浆Ca2+ 过度升高；而MCU的过度增加不仅会加剧胞浆Ca2+ 增高，还会减少线粒体分裂蛋白Drp1和MFF。EA干预后可以抑制MCU的过度表达，促进线粒体重摄取Ca2+ ,逆转胞浆Ca2+ 超载。此外，EA还可以调控线粒体分裂蛋白Drp1和MFF的表达，促进ATP的产生，这有利于多裂肌损伤后线粒体功能的恢复。因此，我们得出结论，EA对布比卡因引起的线粒体功能障碍具有保护作用，这些保护机制可能是通过抑制线粒体内膜的MCU的过度表达，减少肌细胞Ca2+ 超载现象，保护线粒体功能，从而维持肌细胞正常能量需求来实现。.