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目的:研究硒精氨酸(selenoarginine,SeArg)对D-半乳糖(D-gal)所致脑损伤的防护作用。方法:将40只昆明种小鼠随机分成4组:正常组、模型组、低硒剂量组、高硒剂量组。通过后颈背部皮下注射D-半乳糖建立脑损伤模型,以灌胃方式加入SeArg,连续处理6周,采用原子荧光法检测各组小鼠脑Se和血清Se含量,生化分析法检测脑组织匀浆GSH-Px、GSH、SOD、MDA、NO、NOS和血清NO与NOS水平,流式细胞仪检测脑细胞凋亡率,同时对脑组织切片做HE染色及Nissl染色,光镜下观察脑组织病理学变化。结果:与模型组相比,SeArg组小鼠Se、GSH含量和GSH-Px、SOD活性明显上调,MDA、NO含量以及NOS活性显著降低,脑细胞凋亡率明显下调。脑组织染色结果与生化检测结果一致。其中,低剂量的SeArg作用效果更佳。结论:SeArg对D-半乳糖所致的小鼠脑损伤有明显的防护作用,这种保护效应与SeArg能够清除自由基,提高抗氧化酶活性,增强抗氧化防御机制有关。
Objective: To study the protective effect of selenoarginine (SeArg) on brain injury induced by D-galactose (D-gal). Methods: 40 Kunming mice were randomly divided into 4 groups: normal group, model group, low-selenium dose group and high-selenium dose group. The model of traumatic brain injury was established by subcutaneous injection of D-galactose through the back of the neck. Serum was added to SeArg for 6 weeks. The contents of Se and Se in serum were detected by atomic fluorescence spectrometry. The contents of GSH-Px, GSH, SOD, MDA, NO, NOS and the levels of NO and NOS in serum were detected by flow cytometry. The brain sections were stained with HE and Nissl. Pathological changes. Results: Compared with the model group, Se, GSH and GSH-Px and SOD activity in SeArg group were significantly increased, MDA, NO content and NOS activity were significantly decreased, and apoptosis rate of brain cells was significantly decreased. Brain tissue staining results consistent with the biochemical test results. Among them, low-dose SeArg effect better. Conclusion: SeArg has a protective effect on D-galactose-induced brain injury in mice. This protective effect is related to the ability of SeArg to scavenge free radicals, increase antioxidant enzyme activity and enhance antioxidant defense mechanism.