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作 者:杨朔 胡俊华 王亚娟 王吉娜 胡蕾 YANG Shuo;HU Junhua;WANG Yajuan;WANG Ji’na;HU Lei(Nephrology Department,Zhoushan Hospital of Chinese Medicien,Zhoushan,Zhejiang 316000)
出 处:《中国中医药科技》2021年第6期897-900,共4页Chinese Journal of Traditional Medical Science and Technology
基 金:浙江省舟山市科技局项目(2016C31046)。
摘 要:目的:探究雷公藤乙素对糖尿病肾病(DN)大鼠肾组织磷酸化丝裂原活化蛋白激酶p38(p-p38MAPK)、肿瘤坏死因子-α(TNF-α)及白介素-1β(IL-1β)的影响。方法:SD雄性大鼠30只随机分为正常对照组、模型组、雷公藤乙素组,各组均为10只。采用链状佐菌素(STZ)注射方法制作大鼠糖尿病肾病模型,模型成功后,雷公藤乙素组以雷公藤乙素[200μg/(kg·d)]灌胃,正常对照组、模型组予等容积生理盐水灌胃给药,连续给药8周。检测各组大鼠24 h尿蛋白定量及血糖、肌酐、尿素氮水平;光镜观察肾组织病理形态变化,免疫组化检测各组大鼠肾组织TNF-α、IL-1β表达,Western Blot检测肾组织p-p38MAPK蛋白表达。结果:雷公藤乙素组大鼠肾功能指标及蛋白尿较模型组均有明显好转;肾小球系膜细胞增生及肾小管水肿均减轻。TNF-α、IL-1β在正常对照组肾组织表达极少;TNF-α、IL-1β在模型组表达显著增强;雷公藤乙素组TNF-α、IL-1β表达明显低于模型组。模型组肾组织p-p38MAPK表达与正常对照组比较显著增强,雷公藤乙素组较模型组表达减弱。结论:雷公藤乙素能明显改善糖尿病肾病大鼠的肾损伤,其机制可能与减少炎症因子TNF-α、IL-1β的表达,下调肾组织p-p38MAPK的蛋白表达有关。Objective:To investigate the effects of Triptolide on phosphorylated mitogen activated protein kinase p38(P-P38MAPK),IL-1βand TNF-αin renal tissue of diabetic nephropathy(DN)rats.Methods:30 SD rats were randomly divided into normal control,model and Triptolide groups with each 10 rats.The models with diabetic nephropathy were made by injection of STZ.After modeling successfully,the Triptolide group were givenTridiolide[200μg/(kg·d)],and the normal and model groups were given the same volume saline byintragastric administration for 8 weeks.24 hour urine protein,andserum glucose,BUN,SCr were determined,renal tissue pathological morphology changes were observed by optical microscope,TNF-αand IL-1βexpressions in renal tissue were determined by immunohistochemical staining,p-p38MAPK expression in renal tissue was determined by Western blot.Results:The renal function indexes and 24 hour urine protein in Triptolide group rats got better significantly,to compare with model group,renal tissue pathological morphology changes were reduced obviously.The expression of TNF-αand IL-1βin renal tissue of normal group was very little,TNF-αand IL-1βexpressions in renal tissue of model group were significantly increased,those in Triptolide group were significantly lower than that in the model group.The P-P38MAPK expression in renal tissue of model group rats were significantly higher than that in the normal group,and the expression in the Triptolide groupwas weaker than that in the model group.Conclusion:Triptolide can significantly improve renal damage in diabetic nephropathy rats,the mechanism may be related to decrease the expressions of inflammatory cytokines TNF-α,IL-1 and down regulate the expression of P-P38MAPK protein in renal tissue.
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