Uniporter公司
线粒体
胞浆
细胞生物学
线粒体分裂
化学
多裂肌
线粒体通透性转换孔
内分泌学
医学
药理学
内科学
生物
细胞凋亡
程序性细胞死亡
生物化学
病理
腰痛
替代医学
酶
作者
Xia Li,Jun Zhao,Qiaoqiao Lv,Yuan Tian,Li Zhang,Tong Liu
摘要
Abstract 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 Ca 2+ 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 Ca 2+ , reversing the excessive increase in cytoplasmic Ca 2+ . However, the excessive increase in MCU not only aggravated the increased cytoplasmic Ca 2+ 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 Ca 2+ , and reversed cytosolic Ca 2+ 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 Ca 2+ overloading in muscle cells, thereby protecting mitochondrial function and maintaining the normal energy demand of muscle cells.
科研通智能强力驱动
Strongly Powered by AbleSci AI