Volume 42 Issue 8
Aug.  2021
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Shu-hua FANG, Xin-sheng CHEN, Li CAO, Na WANG. Endogenous NO Mediated Stargazin Nitroso Modification in Synaptic Plasticity after Cerebral Ischemia Reperfusion[J]. Journal of Kunming Medical University, 2021, 42(8): 47-53. doi: 10.12259/j.issn.2095-610X.S20210809
Citation: Shu-hua FANG, Xin-sheng CHEN, Li CAO, Na WANG. Endogenous NO Mediated Stargazin Nitroso Modification in Synaptic Plasticity after Cerebral Ischemia Reperfusion[J]. Journal of Kunming Medical University, 2021, 42(8): 47-53. doi: 10.12259/j.issn.2095-610X.S20210809

Endogenous NO Mediated Stargazin Nitroso Modification in Synaptic Plasticity after Cerebral Ischemia Reperfusion

doi: 10.12259/j.issn.2095-610X.S20210809
  • Received Date: 2021-06-14
    Available Online: 2021-08-04
  • Publish Date: 2021-08-04
  •   Objective  To investigate the role of Stargazin-nitroso modification in synaptic plasticity after cerebral ischemia and reperfusion, and to investigate the molecular mechanism of NO regulating AMPAR “trafficking”.  Methods  The rat model of focal cerebral ischemia-reperfusion injury was replicated by the middle cerebral artery occlusion (MCAO) method, and the animal model was interfered with NMDAR inhibitor MK801 and oxidative reductant DTT, respectively. mNSS score was used to detect the neurological function of rats. TTC staining and Western Blot were used to detect the ischemic injury of the brain; TUNEL staining was used to detect the apoptosis of hippocampal neurons in the ischemic side; Griess staining was used to detect the content of NO in the ischemic side of hippocampal tissue, and Western Blot was used to detect the stargazin-nitrogenization modification level and AMPAR protein expression and activation in the hippocampal tissue.  Results  After treatment with MK801 and DTT, the Stargazin-nitroso modification level (P < 0.01) and NO content (P < 0.01) in MCAO/R model were decreased. Phosphorylation of GluR2 in AMPAR subunit was decreased (P < 0.0001); Inhibition of Stargazin’ s nitrosylation modification improved MCAO/ R-induced nerve damage and apoptosis (P < 0.001).  Conclusion  Inhibition of endogenous NO and Stargazin nitrosylation levels promotes synaptic remodeling in the MCAO/R model, possibly by interfering with the GluR2 affinity between Stargazin helper proteins and AMPAR subunit.
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