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- W2783268504 abstract "Background and Purpose Bax inhibitor-1 (BI-1) has been identified as a suppressor of Bax-mediated cell apoptosis by regulation of endoplasmic reticulum stress-induced cell death. However, the role of BI-1 in Early Brain Injury (EBI) after subarachnoid hemorrhage (SAH) remains unclear. In the present study, we aim to explore the neuroprotective functions of BI-1 in EBI after SAH by using models of SAH that induced endovascular perforation in rats. Method The neurological score, brain water content and blood-brain barrier (BBB) permeability were evaluated simultaneously as prognostic indicators. Western blot, RT-PCR and TUNEL staining were performed to study the role and mechanisms of BI-1 in EBI after SAH. Results We found that BI-1 knockdown increased histological injury and the percentages of TUNEL-positive neuron in hippocampal, promoted the expressions of endoplasmic reticulum (ER) stress proteins inositol-requiring enzyme 1α (IRE1α) and TNF receptor-associated factor 2 (TRAF2), and increased the activation levels of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal kinase (JNK) in the hippocampus of SAH rats compared with rats in SAH + vehicle group. Conclusion Our results indicate that BI-1 may participate in the regulation of EBI after SAH by regulating IRE1-JNK pathway. Thus, the results suggest that BI-1 may be a potential therapeutic target for SAH treatment." @default.
- W2783268504 created "2018-01-26" @default.
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- W2783268504 date "2018-01-16" @default.
- W2783268504 modified "2023-09-27" @default.
- W2783268504 title "Bax inhibitor-1 is required for resisting the Early Brain Injury induced by subarachnoid hemorrhage through regulating IRE1-JNK pathway" @default.
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- W2783268504 doi "https://doi.org/10.1080/01616412.2018.1424699" @default.
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