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为了探讨氧化应激在缺血性脑血管病发生中的作用,本实验采用尾静脉注射枯烯氢过氧化物(CHP1:1000稀释,0.20ml)或叔丁基氢过氧化物(t-BHP)可诱发小鼠短暂性脑缺血(TIA)样发作,过氧化氢(H_2O_2)溶液和却氧不能诱发小鼠TIA样发作,但可加强t-BHP的作用,在这一条件下,连续观察80只小鼠8天,这些小鼠均出现TIA样发作,病理检查可见局灶性神经元缺血缺氧样变及血栓样物质形成、心,肺,肝,肾组织未见明显变化,从而对阐明脑缺血样发作的发病机制有重要意义。
In order to investigate the role of oxidative stress in the pathogenesis of ischemic cerebrovascular disease, caudal vein injection of cumene hydroperoxide (CHP1: 1000 dilution, 0.20ml) or t-BHP Induced transient ischemic attack (TIA) in mice, hydrogen peroxide (H_2O_2) solution and oxygen can not induce mouse TIA-like seizures, but can enhance the role of t-BHP, in this condition, the continuous observation of 80 Only mice for 8 days, these mice were TIA-like seizures, pathological examination showed focal neuronal ischemia and anoxia-like changes and thrombus-like substance formation, heart, lung, liver and kidney tissue showed no significant changes, so that It is important to elucidate the pathogenesis of cerebral ischemia-like episodes.