Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy

Figure 8

Sal ameliorates mitochondria-dependent neuronal apoptosis after spinal cord ischemia-reperfusion injury partially through inhibiting oxidative stress and promoting mitophagy. Oxidative stress occurs in spinal cord neurons after I/R or OGD/R, resulting in ROS that damage mitochondria, leading to changes in and the release of large amounts of cytochrome C to induce caspase-mediated endogenous apoptosis. The loss of neurons will eventually lead to impaired neuronal function, such as paralysis. Multiple bioactive drugs including Sal can, on the one hand, reduce the level of damage to mitochondria by inhibiting oxidative stress and can, on the other hand, strengthen PINK1-Parkin pathway-mediated mitophagy in the early stage of spinal cord ischemia-reperfusion injury to accelerate the clearance of damaged mitochondria.