Neuroinflammation and Oxidative Stress in Ischemic Stroke: Molecular Mechanisms and Therapeutic Targets

Ischemic stroke refers to a serious condition causing both paralysis and death. This disorder is caused by interruption of blood flow to the parts of the brain, resulting in destruction of the nerve cells. Secondary injuries inflicted on the brain can occur as a result of neuroinflammation and oxidative stress, causing damage to neurons and threatening the function of the blood–brain barrier (BBB). Both ischemia and reperfusion promote the development of too much reactive oxygen species (ROS) and make mitochondria dysfunctional, which leads to damaging the cells. In addition, activation of microglia causes a release of proinflammatory cytokines, including interleukin-1β, interleukin-6, and tumor necrosis factor-alpha, that aggravate the situation. Together with the conditional processes mentioned above, a disturbance in such processes as nuclear factor kappa B (NF-κB), nuclear factor erythroid 2-related factor 2 (Nrf2), and the inflammasome signaling can help in understanding these intricate connections in order to develop drugs for overcoming ischemia. Using antioxidants, anti-inflammatory drugs, mitochondrial protective agents, and targeted pathways can help fight this disease.