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目的:研究硝酸羟胺染毒后wistar大鼠的脑组织表达血红素氧合酶-1、缺氧诱导因子、突触囊泡蛋白(Synapto-brevin)及突触前膜列阵蛋白(Syntaxin)的表达情况,探讨硝酸羟胺致大鼠缺血性脑损伤的作用机制。方法:利用硝酸羟胺染毒wistar大鼠动物模型,通过免疫化学、免疫荧光、分子原位杂交技术和图像分析技术对缺血缺氧相关蛋白和mRNA及突触囊泡相关蛋白进行定性和定量分析。结果:HAN染毒后6 h～7 d,大脑皮质、海马及小脑细胞HO-1蛋白表达增强,14 d后HO-1逐渐恢复。图像分析结果显示,大脑皮质、海马及小脑HO-1蛋白表达于HAN注射后1 d～3 d均明显高于对照组(P<0.05或P<0.01)。HAN注射后6 h～7 d,脑组织神经元及神经胶质细胞HIF-1蛋白表达均增强,14 d后HIF-1蛋白逐渐恢复;HIF-1 mRNA表达呈类似的变化趋势。图像分析结果显示,大脑皮质、海马及小脑HIF-1蛋白表达于HAN注射后1～7d明显高于对照组(P<0.05或P<0.01)。HAN注射后6 h～7 d,Synaptobrevin 2表达减弱,Syntaxin表达增强,但其聚集减弱,14 d后Synaptobrevin 2及Syntaxin表达逐渐恢复正常。结论:缺血缺氧相关因子(HO-1和HIF-1)的表达上调和突触囊泡相关蛋白(Synaptobrevin 2和Syntaxin)等神经递质释放障碍在HAN致脑损伤中发挥重要作用。
Objective: To study the effects of hydroxylamine on the expression of heme oxygenase-1, hypoxia inducible factor, Synapto-brevin and Syntaxin in brain of wistar rats To investigate the mechanism of hydroxylamine hydrochloride-induced ischemic brain injury in rats. Methods: Animal models of wistar rats were treated with hydroxylamine nitrate, and qualitative and quantitative analysis of proteins associated with ischemia-hypoxia and mRNA and synaptic vesicle-associated proteins were performed by immunochemistry, immunofluorescence, molecular in situ hybridization and image analysis . Results: The expression of HO-1 protein in cerebral cortex, hippocampus and cerebellum increased from 6 h to 7 d after HAN exposure, and gradually recovered after 14 d. The results of image analysis showed that the expression of HO-1 protein in cerebral cortex, hippocampus and cerebellum were significantly higher than those in control group (P <0.05 or P <0.01) on the 1st and 3rd day after HAN injection. The expression of HIF-1 protein in brain tissue neurons and glial cells increased from 6 h to 7 d after HAN injection, and gradually recovered after 14 d. The expression of HIF-1 mRNA showed a similar trend. The results of image analysis showed that the expression of HIF-1 in cerebral cortex, hippocampus and cerebellum was significantly higher than that of the control group (P <0.05 or P <0.01) 1 to 7 days after HAN injection. The expression of Synaptobrevin 2 was weakened and the expression of Syntaxin was enhanced 6 h ~ 7 d after HAN injection. However, the expression of Synaptobrevin 2 and Syntaxin gradually returned to normal after 14 d. CONCLUSION: Upregulation of hypoxia and hypoxia related factors (HO-1 and HIF-1) and neurotransmitter release disorders such as Synaptobrevin 2 and Syntaxin play an important role in HAN-induced brain injury.