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目的为了探讨20-羟基蜕皮甾酮(20E)对2型糖尿病大鼠神经细胞的影响及相关机制。方法大鼠造模结束后,将造模成功大鼠分为模型组、二甲双胍组和20E治疗组。正常组和模型组灌服蒸馏水,二甲双胍照组和20E治疗组分别灌胃5 mg/kg盐酸二甲双胍和10 mg/kg 20E溶液。药物干预6周后,HE染色观察海马的形态学变化,real-time PCR分析海马超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和核因子кB的表达,ELISA测定脑组织脑源性神经因子和转化生长因子-β1的水平。结果与模型组相比,20E处理后海马细胞损伤程度减轻,海马中超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶m RNA水平显著增加,核因子кB表达水平明显降低,脑组织脑源性神经因子含量增加。结论 20E具有减轻2型糖尿病大鼠海马细胞损伤的作用,其机制可能与提高脑组织组织抗氧化能力有关。
Objective To investigate the effects of 20-hydroxyecdysone (20E) on neurons in type 2 diabetic rats and the related mechanisms. Methods After modeling, rats were divided into model group, metformin group and 20E treatment group. Normal group and model group were fed with distilled water. Metformin group and 20E treatment group were given 5 mg / kg metformin hydrochloride and 10 mg / kg 20E solution respectively. Six weeks after the drug intervention, the morphological changes of the hippocampus were observed by HE staining. The levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and nuclear factor кB, and the levels of brain-derived brain-derived neurotrophic factor and transforming growth factor-β1 were measured by ELISA. Results Compared with the model group, the injury of hippocampal cells in 20E group was alleviated. The levels of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase m RNA in hippocampus were significantly increased The expression of factor кB was significantly decreased, and the content of brain-derived neurotrophic factor increased. Conclusion 20E can relieve the damage of hippocampal cells in type 2 diabetic rats. The mechanism may be related to the enhancement of antioxidant capacity in brain tissues.