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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 and mechanism of iron ion in cerebral hemorrhage injury. Methods The right basal ganglion of SD rats was injected with 30μl of autologous thawed red blood cells. After 24 hours, the levels of heme oxygenase-1 (HO-1), non-heme iron ion concentration, superoxide dismutase (SOD) activity, DNA single strand injury [naked end labeling staining (PANT staining) ] And oxidative damage markers, and to further observe the protective effect of deferoxamine on brain tissue. Results Injection into the right basal ganglia of SD rats resulted in loss of neurological function, increased local brain edema and HO-1 levels, and non-heme iron retention in the brain. Accompanied by a significant decrease in SOD activity, a large number of PANT positive cells around the hematoma. After deferoxamine intervention, the levels of non-heme iron decreased significantly, and neurological signs and brain edema improved at the same time. Conclusion Erythrocyte melting caused brain tissue injury, iron retention in brain tissue and through the mechanism of peroxidation is one of the key factors causing injury. Deferoxamine removal of iron ions can reduce the destruction of tissue damage caused by the melting of red blood cells.