Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Abstract

Hemorrhagic stroke is a common and severe neurological disorder and is associated with high rates of mortality and morbidity, especially for intracerebral hemorrhage (ICH). Increasing evidence demonstrates that oxidative stress responses participate in the pathophysiological processes of secondary brain injury (SBI) following ICH. The mechanisms involved in interoperable systems include endoplasmic reticulum (ER) stress, neuronal apoptosis and necrosis, inflammation, and autophagy. In this review, we summarized some promising advances in the field of oxidative stress and ICH, including contained animal and human investigations. We also discussed the role of oxidative stress, systemic oxidative stress responses, and some research of potential therapeutic options aimed at reducing oxidative stress to protect the neuronal function after ICH, focusing on the challenges of translation between preclinical and clinical studies, and potential post-ICH antioxidative therapeutic approaches.

Figure 1

Schematic representation of major intracellular pathway in the role of reactive oxygen species radicals in hemorrhagic stroke. ROS: Reactive oxygen species; RNS: reactive nitrogen species; ICH: intracerebral hemorrhage; ER stress: endoplasmic reticulum stress; BBB: blood brain barrier.