An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.

Fa Lin,Xiaolin Chen,Yu Chen,Wen-Jun Tu,Jizong Zhao,Runting Li,Ke Wang

doi:10.3389/fnagi.2021.772036

Abstract

The main reasons for disability and death in aneurysmal subarachnoid hemorrhage (aSAH) may be early brain injury (EBI) and delayed cerebral ischemia (DCI). Despite studies reporting and progressing when DCI is well-treated clinically, the prognosis is not well-improved. According to the present situation, we regard EBI as the main target of future studies, and one of the key phenotype-oxidative stresses may be called for attention in EBI after laboratory subarachnoid hemorrhage (SAH). We summarized the research progress and updated the literature that has been published about the relationship between experimental and clinical SAH-induced EBI and oxidative stress (OS) in PubMed from January 2016 to June 2021. Many signaling pathways are related to the mechanism of OS in EBI after SAH. Several antioxidative stress drugs were studied and showed a protective response against EBI after SAH. The systematical study of antioxidative stress in EBI after laboratory and clinical SAH may supply us with new therapies about SAH.

Highlights

Aneurysmal subarachnoid hemorrhage is a devastating disease, mainly induced by the rupture of an intracranial aneurysm and linked to high levels of morbidity and mortality (Bor et al, 2008; Connolly et al, 2012; Macdonald and Schweizer, 2017; Chao et al, 2021)
The oxidative stress (OS) responses include a wide variety of active and inactive substances, which play a substantial role in early brain injury (EBI) after aneurysmal subarachnoid hemorrhage (aSAH) and may be associated with delayed cerebral ischemia (DCI) and long-term outcomes (Cahill et al, 2006; Rowland et al, 2012; Sehba et al, 2012; Shao et al, 2020)
Melatonin inhibits the disruption of tight junction proteins possibly linked to the adjustment of proinflammatory cytokines (Chen et al, 2014a). These results demonstrate that regulation of melatonin attenuates symptomatic dysfunction (Chen et al, 2015)

Summary

Introduction

Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease, mainly induced by the rupture of an intracranial aneurysm and linked to high levels of morbidity and mortality (Bor et al, 2008; Connolly et al, 2012; Macdonald and Schweizer, 2017; Chao et al, 2021). Nrf2-ARE pathway is activated in the brain after SAH, playing a beneficial role in EBI development, possibly through inhibiting cerebral oxidative stress by inducing antioxidant and detoxifying enzymes TSG-6 attenuated oxidative stress and apoptosis in EBI after SAH partly by inhibiting NF-κB and activating HO-1 pathway in brain tissue

Results

Conclusion