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作 者:毛竹君 张芯 张璐 王晓倩[1] 张广顺[1] MAO Zhu-jun;ZHANG Xin;ZHANG Lu;WANG Xiao-qian;ZHANG Guang-shun(College of Pharmaceutical Sciences,Zhejiang Chinese Medical University,Hangzhou 310053,China)
出 处:《中华中医药杂志》2020年第9期4672-4675,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:国家自然科学基金项目(No.81603351);浙江中医药大学科研基金人才专项项目(No.2019ZR14);浙江中医药大学药学院时珍青年项目(No.SZZ201815)。
摘 要:目的:探究运脾活血散结方对2型糖尿病大鼠血管内皮损伤的影响及其相关的作用机制。方法:将Wistar大鼠随机分为3组:正常对照组、糖尿病模型组、运脾活血散结方组。应用硝酸还原酶法检测血清NO水平,酶联免疫吸附试验(ELISA)检测血清IL-6水平,Western Blot分析Akt、pAkt^ser473、eNOS和peNOS^ser632蛋白表达水平。结果:与正常对照组比较,糖尿病模型组pAkt^ser473、peNOS^ser632蛋白表达及血清NO水平显著降低(P<0.05),血清IL-6水平显著升高(P<0.05);与糖尿病模型组比较,运脾活血散结方组pAkt^ser473、peNOS^ser632蛋白表达水平及血清NO水平显著升高(P<0.05),血清IL-6水平显著下降(P<0.05)。结论:运脾活血散结方激活PI3K/Akt/eNOS通路,提高血清NO水平,降低血清IL-6水平,可能是其抗2型糖尿病血管内皮损伤的部分作用机制。Objective:To investigate the effects of Yunpi Huoxue Sanjie Decoction on vascular endothelial injury of type 2 diabetes mellitus(T2 DM)rats and explore the undering mechanisms.Methods:Wistar rats were randomly divided into three groups:control group,diabetes group,Yunpi Huoxue Sanjie Decoction group.The serum concentration of NO was detected by Nitralereduetase method.The serum concentration of IL-6 was detected by ELISA.The expression of Akt,pAkt^ser473,eNOS and peNOS^ser632 were analyzed by Western Blot.Results:Compared with control group,the expression of pAkt^ser473,peNOS^ser632 and NO were significantly down-regulated,and IL-6 were significantly up-regulated in diabetes group(P<0.05).Compared with diabetes group,the expression of pAkt^ser473,peNOS^ser632 and NO were significantly up-regulated(P<0.05),and IL-6 were significantly down-regulated in Yunpi Huoxue Sanjie Decoction group(P<0.05).Conclusion:Yunpi Huoxue Sanjie Decoction can inhibit vascular endothelial injury by activating PI3 K/Akt/eNOS pathway to up-regulate the serum concentration of NO and down-regulate the serum concentration of IL-6.
关 键 词:运脾活血散结方 2型糖尿病 血管内皮损伤 PI3K/Akt/eNOS通路
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