2. Academic Validation
  3. Tat-NR2B9c attenuates oxidative stress via inhibition of PSD95-NR2B-nNOS complex after subarachnoid hemorrhage in rats

Tat-NR2B9c attenuates oxidative stress via inhibition of PSD95-NR2B-nNOS complex after subarachnoid hemorrhage in rats

  • Neuropharmacology. 2024 Mar 21:109905. doi: 10.1016/j.neuropharm.2024.109905.
Haocheng Zhang 1,  Longbiao Xu 2,  Yezhao He 1,  Zeyu Zhang 3,  Jiahao Zhang 1,  Qian Yu 1,  Yibo Liu 1,  Xiaoyu Wang 1,  Anke Zhang 1,  Kaikai Wang 1,  Yuanjian Fang 4,  Sheng Chen 5
Affiliations

Affiliations

  • 1 Department of Neurosurgery, School of Medicine, The Second Affiliated Hospital, Zhejiang University, Zhejiang Province, Hangzhou, China; Key Laboratory of Precise Treatment and Clinical Translational Research of Neurological Diseases, Hangzhou, Zhejiang, China.
  • 2 Department of Neurosurgery, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
  • 3 Department of Neurosurgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, China.
  • 4 Department of Neurosurgery, School of Medicine, The Second Affiliated Hospital, Zhejiang University, Zhejiang Province, Hangzhou, China; Key Laboratory of Precise Treatment and Clinical Translational Research of Neurological Diseases, Hangzhou, Zhejiang, China. Electronic address: sandman0506@zju.edu.cn.
  • 5 Department of Neurosurgery, School of Medicine, The Second Affiliated Hospital, Zhejiang University, Zhejiang Province, Hangzhou, China; Key Laboratory of Precise Treatment and Clinical Translational Research of Neurological Diseases, Hangzhou, Zhejiang, China. Electronic address: saintchan@zju.edu.cn.
PMID: 38521229 DOI: 10.1016/j.neuropharm.2024.109905
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.

Keywords

Oxidative stress; Postsynaptic density protein-95; Subarachnoid hemorrhage; Tat-NR2B9c.

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