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白藜芦醇防治糖尿病肾病与抑制肾脏炎症和系膜细胞增殖有关:Akt/NF-κB 通路的可能作用。

Resveratrol Prevention of Diabetic Nephropathy Is Associated with the Suppression of Renal Inflammation and Mesangial Cell Proliferation: Possible Roles of Akt/NF-κB Pathway.

机构信息

Department of Nephrology, The Second Hospital of Jilin University, 218 Ziqiang Street, Changchun 130041, China.

Department of Cardiology, The Second Hospital of Jilin University, 218 Ziqiang Street, Changchun 130041, China.

出版信息

Int J Endocrinol. 2014;2014:289327. doi: 10.1155/2014/289327. Epub 2014 Feb 9.

Abstract

The present study was to investigate the protection of resveratrol (RSV) in diabetes associated with kidney inflammation and cell proliferation. Rat mesangial cell and streptozotocin-induced type 1 diabetes mouse model were used. In vitro, RSV attenuated high glucose-induced plasminogen activator inhibitor (PAI-1) expression and mesangial cell proliferation, as well as Akt and nuclear factor-kappa B (NF- κ B) activation. The similar results were recaptured in the experiment with Akt inhibitors. In vivo, mice were divided into three groups: control group, diabetes mellitus (DM) group, and RSV-treated DM group. Compared with control group, the kidney weight to body weight ratio and albumin to creatinine ratio were increased in DM group, but not in RSV-treated DM group. Furthermore, the increased expression of PAI-1 and intercellular adhesion molecule-1 in diabetic renal cortex were also reduced by RSV administration. Besides, the kidney p-Akt/Akt ratio and NF- κ B were significantly increased in DM group; however, these changes were reversed in RSV-treated DM group. Additionally, immunohistochemistry results indicated that RSV treatment reduced the density of proliferating cell nuclear antigen-positive cells significantly in glomeruli of diabetic mice. These results suggest that RSV prevents diabetes-induced renal inflammation and mesangial cell proliferation possibly through Akt/NF- κ B pathway inhibition.

摘要

本研究旨在探讨白藜芦醇(RSV)在糖尿病相关肾炎症和细胞增殖中的保护作用。采用大鼠肾小球系膜细胞和链脲佐菌素诱导的 1 型糖尿病小鼠模型。体外,RSV 减弱了高糖诱导的纤溶酶原激活物抑制剂(PAI-1)表达和系膜细胞增殖,以及 Akt 和核因子-κB(NF-κB)的激活。在 Akt 抑制剂的实验中也观察到了类似的结果。在体内,将小鼠分为三组:对照组、糖尿病(DM)组和 RSV 治疗的 DM 组。与对照组相比,DM 组的肾脏重量与体重比和白蛋白与肌酐比增加,但 RSV 治疗的 DM 组没有增加。此外,RSV 给药可降低糖尿病肾皮质中 PAI-1 和细胞间黏附分子-1 的表达增加。此外,DM 组肾脏 p-Akt/Akt 比值和 NF-κB 显著增加;然而,这些变化在 RSV 治疗的 DM 组中得到逆转。此外,免疫组织化学结果表明,RSV 治疗可显著降低糖尿病小鼠肾小球中增殖细胞核抗原阳性细胞的密度。这些结果表明,RSV 通过抑制 Akt/NF-κB 通路预防糖尿病引起的肾炎症和系膜细胞增殖。

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