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目的:阐明诱导型一氧化氮(NO)信号通路在代谢型谷氨酸受体2/3(mGluR2/3)参与海马脑缺血预处理(CIP)保护机制中的作用。方法:本实验采用免疫组化,观察脑室应用mGluR2/3阻断剂α-甲基-(4 -四唑基-苯)甘氨酸(MTPG)对CIP诱导的iNOS表达的影响。36只永久凝闭椎动脉的SD大鼠随机分为sham、CIP、损伤性缺血、CIP +损伤性缺血、MTPG+CIP和MTPG+CIP +损伤性缺血6组,每组6只。各组大鼠均在术后或末次缺血再灌后,常温饲养5 d取材观察。结果:Sham组胞浆有较弱的iNOS表达。CIP组和CIP +损伤性缺血组NOS表达与sham组相比明显增加。在CIP前20 min脑室注射mGluR2/3阻断剂MTPG,可阻断CIP引起的iNOS表达增加,但对神经元的形态无影响。而MTPG+CIP +损伤性缺血组中,iNOS的表达较MTPG+CIP组明显增加,同时锥体神经元的轮廓、形态出现明显的损伤性改变。结论:CIP能够引起一定程度的iNOS表达增加,而MTPG能阻断CIP引起的iNOS的表达增加,同时又能阻断CIP抗后续损伤性缺血的作用,提示iNOS信号通路在mGluR2/3介导的脑缺血耐受过程中发挥重要作用。
OBJECTIVE: To elucidate the role of inducible nitric oxide (NO) signaling in the protection of hippocampus cerebral ischemic preconditioning (CIP) by metabotropic glutamate receptor 2/3 (mGluR2 / 3). Methods: The effects of mGluR2 / 3 blocker α - methyl - (4 - tetrazolyl - phenyl) glycine (MTPG) on CIP - induced iNOS expression in the ventricles were observed by immunohistochemistry. Thirty-six permanent vertebral arteries were randomly divided into sham, CIP, ischemic insult, CIP + ischemic insult, MTPG + CIP and MTPG + CIP + ischemic insult 6 rats in each group. Rats in each group were given postoperative or last ischemia and reperfusion at room temperature for 5 days. Results: Weak iNOS expression in cytoplasm of Sham group. Compared with sham group, the expression of NOS in CIP group and CIP + ischemic group increased significantly. Intraventricular injection of mGluR2 / 3 blocker MTPG 20 min before CIP blocked the increase of iNOS induced by CIP, but had no effect on the morphology of neurons. In MTPG + CIP + ischemic insult group, the expression of iNOS was significantly increased compared with MTPG + CIP group, meanwhile, the morphological changes of pyramidal neurons were obviously damaged. CONCLUSION: CIP can induce a certain degree of iNOS expression increase, while MTPG can block the increase of iNOS induced by CIP, and at the same time, it can block the effect of CIP on subsequent ischemic injury, suggesting that iNOS signaling pathway is mediated by mGluR2 / 3 The process of cerebral ischemic tolerance plays an important role.