跑台运动通过增强Caveolin-1保护线粒体功能减轻脑缺血损伤

Abstract

Aims Exercise training has a neuroprotective effect against ischaemic injury, but the underlying mechanism is not completely clear. This study explored the potential mechanisms underlying the protective effects of treadmill training and caveolin-1 regulation against mitochondrial dysfunction in cerebral ischaemic injury. Main methods After middle cerebral artery occlusion (MCAO) surgery, rats were subjected to treadmill training and received daidzein injections and combined therapy. A series of analyses, including neurological function scoring; body weight measurement; Nissl, haematoxylin and eosin staining; cerebral infarction volume assessment; mitochondrial morphology examination; caveolin-1, cytoplasmic and mitochondrial cytochrome C (Cyt C), and translocase of outer membrane 20 (TOM20) expression analysis; apoptosis index analysis; and transmission electron microscopy were conducted. Key findings Treadmill training increased caveolin-1 expression, reduced neurobehavioral scores and cerebral infarction volumes, improved tissue morphology, reduced neuronal loss, inhibited mitochondrial outer membrane permeabilization (MOMP) through the caveolin-1 pathway, prevented excessive Cyt-C release from mitochondria, and reduced the degrees of apoptosis and mitochondrial damage. In addition, treadmill training increased the expression of TOM20 through the caveolin-1 pathway and maintained import signal function, thereby protecting mitochondrial integrity. Significance Treadmill exercise protected mitochondrial integrity and inhibited the endogenous mitochondrial apoptosis pathway. The damage of cerebral ischaemia was alleviated in rats through enhancement of caveolin-1 by treadmill exercise.