1. Tat-NR2B9c attenuates oxidative stress via inhibition of PSD95-NR2B-nNOS complex after subarachnoid hemorrhage in rats.
- Author
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Zhang, Haocheng, Xu, Longbiao, He, Yezhao, Zhang, Zeyu, Zhang, Jiahao, Yu, Qian, Liu, Yibo, Wang, Xiaoyu, Zhang, Anke, Wang, Kaikai, Fang, Yuanjian, and Chen, Sheng
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SUBARACHNOID hemorrhage , *RATS , *BAX protein , *OXIDATIVE stress , *BCL-2 proteins , *BRAIN injuries , *PROTEIN expression - Abstract
Oxidative stress plays important roles in the pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Tat-NR2B9c has shown efficacy as a neuroprotective agent in several studies. Here, we identified the neuroprotective role of Tat-NR2B9c after SAH and its related mechanisms. The results showed that Tat-NR2B9c treatment attenuated oxidative stress, therefore alleviated neuronal apoptosis and neurological deficits after SAH. Tat-NR2B9c treatment could alleviate mitochondrial vacuolization induced by SAH. Compared to SAH + vehicle group, Tat-NR2B9c resulted in the decrease of Acetylated superoxide dismutase2 (Ac-SOD2), Bcl-2-associated X protein (Bax) and cleaved-caspase3 (CC3) protein expression, and the up-regulation of Sirtunin 3 (Sirt3) and Bcl-2 protein level. Moreover, Tat-NR2B9c attenuated excitotoxicity by inhibiting the interaction of PSD95-NR2B-nNOS. Our results demonstrated that Tat-NR2B9c inhibited oxidative stress via inhibition of PSD95-NR2B-nNOS complex formation after SAH. Tat-NR2B9c may serve as a potential treatment for SAH induced brain injury. • Oxidative stress is one of the important mechanisms of EBI after SAH. • Tat-NR2B9c protects neurological deficits by decreasing oxidative stress after SAH. • Tat-NR2B9c reduces PSD95-NR2B-nNOS complex formation after SAH. • Tat-NR2B9c could be used as a novel candidate for SAH treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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