Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy.
Xiaochun DuanZunjia WenHaitao ShenMeifen ShenHeng GaoPublished in: Oxidative medicine and cellular longevity (2016)
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.
Keyphrases
- oxidative stress
- brain injury
- cerebral ischemia
- subarachnoid hemorrhage
- diabetic rats
- ischemia reperfusion injury
- induced apoptosis
- dna damage
- endoplasmic reticulum
- endothelial cells
- atrial fibrillation
- cell death
- early onset
- type diabetes
- cell proliferation
- cardiovascular disease
- stem cells
- cell therapy
- drug induced
- pluripotent stem cells