FIGURE 7.

A schematic representation of the proposed mechanism between oxidative stress and mitochondrial dysfunction in cerebral ischemic reperfusion injury. Excessive oxidative stress and mitochondrial dysfunction are fundamental contributors to neuronal injury in cerebral ischemic reperfusion injury (A). Ischemic/reperfusion condition induces calcium overload, which results in calcium influx into mitochondria and mitochondrial permeability transition pore (PTP) opening. Meanwhile, accumulation of intermediate succinate results from reverse electron transport from mitochondrial complex II to complex I. These changes contribute to ROS burst in the neuron. The excessive ROS reversely leads to PTP opening and forms a vicious circle in cerebral ischemic reperfusion injury (B). Our study provides evidence that the impaired oxidant/antioxidant balance and mitochondrial dysfunction could be rescued by OM-MSC treatment (C). Collectively, OM-MSC implantation is a promising approach for the management of cerebral ischemic reperfusion injury.