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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Inhibition of phosphorylation of p38 MAPK involved in the protection of nephropathy by emodin in diabetic rats.
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Inhibition of phosphorylation of p38 MAPK involved in the protection of nephropathy by emodin in diabetic rats.

机译：大黄素抑制大黄素参与糖尿病大鼠肾脏p38 MAPK磷酸化的保护作用。

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摘要

To explore the protection of emodin on renal dysfunction in the streptozotocin-induced diabetic rats with nephropathy and the role of p38 mitogen-activated protein kinase (p38 MAPK) signal transduction pathway in this protection. 30 male Spraque-Dawley rats were randomly divided into control group, model group and emodin group. The rats in the model group and emodin group were administered with streptozotocin (60 mg/kg) to induce diabetes. 40 mg/kg/day of emodin were orally given to the rats in emodin group. The rats in other groups were only given solvent. Biochemical index were analysed by oxidase and oxidase dynamical enzyme method. Glomerular area and volume were determined quantitatively by using Image Analysis System. Western blotting and immunohistochemical staining was used to detect the total p38 MAPK, phosphorylated p38 MAPK, phosphorylated cAMP response element binding protein (CREB) and fibronectin. The average kidney weight/body weight, glomerular area, glomerular volume and all biochemical indexes significantly increased in model group as compared to the control group (P<0.05), while the average body weight decreased. The expressions of phosphorylaed p38 MAPK, phosphorylated CREB and fibronectin increased by 1.98-fold, 1.94-fold and 1.96-fold respectively in model group compared with those in the control group (P<0.05). Emodin markedly decreased the average kidney weight/body weight, glomerular area, glomerular volume and all biochemical indexes (P<0.05), having a weak action on the level of blood glucose. The expressions of phosphorylated p38 MAPK, phosphorylated CREB and fibronectin also significantly downregulated in emodin group compared with those in model group (P<0.05). Emodin was efficient to ameliorate renal dysfunction in diabetic nephropathy rats probably by its inhibition of the activation of p38 MAPK pathway and downregulation of the expression of fibronectin.
机译：探讨大黄素对链脲佐菌素诱发的糖尿病肾病大鼠肾脏功能的保护作用，以及p38促分裂原激活蛋白激酶（p38 MAPK）信号转导通路在这种保护中的作用。将30只雄性Spraque-Dawley大鼠随机分为对照组，模型组和大黄素组。给模型组和大黄素组的大鼠注射链脲佐菌素（60 mg / kg）以诱发糖尿病。大黄素组大鼠口服大黄素40 mg / kg / day。其他组只给予溶剂。用氧化酶和氧化酶动态酶法分析生化指标。使用图像分析系统定量测定肾小球的面积和体积。免疫印迹和免疫组化染色用于检测总的p38 MAPK，磷酸化的p38 MAPK，磷酸化的cAMP反应元件结合蛋白（CREB）和纤连蛋白。模型组与对照组相比，平均肾重/体重，肾小球面积，肾小球体积和所有生化指标显着增加（P <0.05），而平均体重却下降。与对照组相比，模型组磷酸化的p38 MAPK，磷酸化的CREB和纤连蛋白的表达分别增加了1.98倍，1.94倍和1.96倍（P <0.05）。大黄素显着降低了平均肾脏重量/体重，肾小球面积，肾小球体积和所有生化指标（P <0.05），对血糖水平的作用较弱。大黄素组磷酸化的p38 MAPK，磷酸化的CREB和纤连蛋白的表达也明显低于模型组（P <0.05）。大黄素可能通过抑制p38 MAPK途径的激活和下调纤连蛋白的表达而有效改善糖尿病肾病大鼠的肾功能不全。

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