Using complex II as an emerging therapeutic target for the treatment of muscle lesions.

After patients has been trapped into skeletal muscle injury, hypoxic and dysfunctional mitochondria brings about a crisis in energy supply that severely disrupts the repair of skeletal muscle. This study aims to elucidate injury-induced adaptations in the mitochondria and provide statistics for the role of complex II in instilling cells with energy under hypoxic conditions. Fifty-six male Wistar rats were divided into control, 12 h, 2 d, 5 d, 7 d, 10 d, 15 d, and 30 d postinjury groups. Contusion injury was made via an instrumented drop-mass technique delivering single impact to the posterior surface of the gastrocnemius of one limb of the rats. ROS levels, loss of mitochondrial membrane potential (MMP), activities of marker enzymes (miCK, LDH, and ALP), and activities of complexes I-III were determined. Our findings reveal that the first 2 d postinjury, especially at 12 h, is the period with most severe oxidative stress. After injury, the activities of mitochondrial complexes I-III display different behaviors based on time and various energy production mechanisms. Our results highlight that complex II participates in electron transport in the acute phase of blunt trauma. We proposed that CII could be a therapeutic target in muscle lesions.