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作 者:吴继敏[1] 王爽[1] 闻树群[1] 王也玲[1] 宋水江[1]
机构地区:[1]浙江大学医学院附属第二医院神经内科,浙江省杭州310009
出 处:《中华急诊医学杂志》2005年第7期563-566,共4页Chinese Journal of Emergency Medicine
摘 要:目的探讨铁离子在脑出血损伤中的作用和机制。方法SD大鼠右侧基底节注射自体融解红细胞30μl。24h后观察神经、血红素加氧酶-1水平(HO-1)、非血红素铁离子浓度、超氧化物岐化酶(SOD)活性、DNA单链损伤[裸露末端标记染色(PANT染色)]和氧化损伤标记物,并进一步观察去铁敏对脑组织的保护作用。结果SD大鼠右侧基底节注射30μl融解红细胞24h后造成神经功能缺失,局部脑水肿和HO-1水平增高,及脑内非血红素铁离子潴留。伴随SOD活性的显著性下降,血肿周围出现大量PANT阳性细胞。去铁敏干预后,非血红素铁离子水平显著下降,神经体征和脑水肿同时得到改善。结论红细胞融解后引起脑组织损伤,铁离子在脑组织中的潴留并通过过氧化机制是引起损伤的关键因素之一。去铁敏清除铁离子可以减轻融解红细胞产生的对组织的破坏。Objective To investigate the role of and mechanism of injuries during intracerebral hemorrhage(ICH).Methods 30 μl of lysed erythrocytes (LEs)from the femoral artery were injected into right basal ganglia of SD rats. Neurological deficits, brain edema, DNA single-strand breaks(SSBs), activity of SOD, heme-oxygenase-1(HO-1) and the level of non-heme iron, one of the breakdown products of hemoglobin,were observed after 24 hours. The effects of iron chelator defroxamine on brain edema and behavior test were also observed. Results Infusion of LEs induced prominent brain edema and neurological deficit after 24 hours. HO-1 was upregulated to 12.5 folds as that in the sham group with retention of non-heme iron in the ipsilateral area of the brain. Positive cells existed around the hematoma by PANT staining,and this indicated SSBs. The activities of CuZn-SOD and Mn-SOD decreased. With the treatment of defroxamine, the concentration of non-heme iron and brain edema decreased significantly, and brain edema and neurological function were improved. Conclusion Erythrocytes, a component of hematoma, can cause the damage of brain tissue after lysis. The retention of non-heme iron because of the degeneration of hemoglobin and the oxidative injury may be key to the pathogentic process. Chelating iron with defroxamine could play an protective role on LEs model.
关 键 词:脑出血 损伤机制 血红素加氧酶-1 超氧化物岐化酶 DNA单链损伤 右侧基底节 神经功能缺失 SD大鼠 铁离子浓度 SOD活性 脑组织损伤 红细胞 去铁敏 氧化损伤 标记染色 保护作用 HO-1 阳性细胞 血肿周围 离子水平 血红素铁
分 类 号:R743.34[医药卫生—神经病学与精神病学] R722.17[医药卫生—临床医学]
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