The Protective Effect of Beraprost Sodium on Diabetic Nephropathy by Inhibiting Inflammation and p38 MAPK Signaling Pathway in High-Fat Diet/Streptozotocin-Induced Diabetic Rats.

The Protective Effect of Beraprost Sodium on Diabetic Nephropathy by Inhibiting Inflammation and p38 MAPK Signaling Pathway in High-Fat Diet/Streptozotocin-Induced Diabetic Rats.
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贝前列素钠抑制高脂饮食/链脲佐菌素诱导的糖尿病大鼠炎症和 p38 MAPK 信号通路对糖尿病肾病的保护作用

DOI:
10.1155/2016/1690474
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发表时间:
2016
影响因子:
2.8
通讯作者:
Liu Z
Liu Z
中科院分区:
医学4区
文献类型:
--
作者:
Peng L;Li J;Xu Y;Wang Y;Du H;Shao J;Liu Z

文献摘要

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背景p38丝裂原活化蛋白激酶(MAPK)在调节与导致糖尿病肾病(DN)的炎症过程有关的信号通路中起关键作用。本研究旨在检测糖尿病肾病(DN)中p38 MAPK的活化情况,并探讨贝前列素钠(BPS)是否通过抑制炎症和p38 MAPK信号通路来改善DN。方法. 40只雄性SD大鼠随机分为正常对照组、2型糖尿病组和BPS治疗组。8周后检测肾脏病理改变、p38 MAPK信号通路激活及炎症反应。结果. BPS治疗后,肾功能、24 h尿蛋白定量、血脂、血糖水平明显改善,肾脏炎症反应减轻,p38 MAPK信号通路表达减弱。结论. BPS对2型糖尿病肾损害有明显的保护作用。其保护机制是复杂的,但可能主要归因于抑制p38 MAPK信号通路和糖尿病肾脏中的炎症。
Background. p38 mitogen-activated protein kinase (MAPK) plays a crucial role in regulating signaling pathways implicated in inflammatory processes leading to diabetic nephropathy (DN). This study aimed to examine p38 MAPK activation in DN and determine whether beraprost sodium (BPS) ameliorates DN by inhibiting inflammation and p38 MAPK signaling pathway in diabetic rats. Methods. Forty male Sprague Dawley (SD) rats were randomly divided into the normal control group, type 2 diabetic group, and BPS treatment group. At the end of the 8-week experiment, we measured renal pathological changes and the activation of the p38 MAPK signaling pathway and inflammation. Result. After BPS treatment, renal function, 24-hour urine protein, lipid profiles, and blood glucose level were improved significantly; meanwhile, inflammation and the expression of p38 MAPK signaling pathway in the diabetic kidney were attenuated. Conclusions. BPS significantly prevented type 2 diabetes induced kidney injury characterized by renal dysfunction and pathological changes. The protective mechanisms are complicated but may be mainly attributed to the inhibition of the p38 MAPK signaling pathway and inflammation in the diabetic kidney.