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目的探讨脑梗死模型中酸性环境能否介导皮质神经元损伤及阻断酸敏感离子通道1α(acidsensing ion channels1α,ASIC1α)的神经保护作用。方法制作缺氧细胞模型、脑梗死动物模型,检测ASIC1α阻断剂对乳酸脱氢酸(lactate dehydrogenase,LDH)释放率、大鼠行为学、脑梗死体积以及ASIC1蛋白表达的影响。结果酸性环境可以损伤皮质神经元,加重缺氧对细胞的毒性作用,经侧脑室注射ASIC1α阻断剂可以改善脑梗死大鼠的行为学改变,梗死体积明显减小(P<0.05);随梗死时间延长,缺血半暗带ASIC1表达增加,在缺血后24h表达量较明显。结论酸性环境导致皮质神经元损伤,其损伤机制与缺血后神经元ASIC1α开放以及表达增加有关;阻断ASIC1α具有神经保护作用。
Objective To investigate the neuroprotective effect of acidic environment on cortical neurons and block acid-sensing ion channels 1α (ASIC1α) in cerebral infarction model. Methods The hypoxic cell model and the model of cerebral infarction were made. The effects of ASIC1α blockers on the release rate of lactate dehydrogenase (LDH), the behavior of rats, the volume of cerebral infarction and the expression of ASIC1 protein were detected. Results The acidic environment could injure the cortical neurons and aggravate the cytotoxic effect of hypoxia. The intracerebroventricular injection of ASIC1α antagonist could improve the behavioral changes of cerebral infarction rats and decrease the infarct volume significantly (P <0.05) With prolonged time, the expression of ASIC1 in penumbra increased, and the expression of ASIC1 was more obvious 24h after ischemia. Conclusion The acidic environment leads to the damage of cortical neurons. The mechanism of injury is related to the opening of ASIC1α and the increase of the expression of ASIC1α in ischemic neurons. Blocking ASIC1α has the neuroprotective effect.