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重组抗IL-6R融合蛋白通过抑制JAK2/STAT3信号通路对糖尿病肾病的肾脏保护作用

Renoprotective Effect of the Recombinant Anti-IL-6R Fusion Proteins by Inhibiting JAK2/STAT3 Signaling Pathway in Diabetic Nephropathy.

作者信息

Zhang Nanwen, Zheng Qingmei, Wang Yaduan, Lin Juan, Wang He, Liu Rui, Yan Mengru, Chen Xiaofeng, Yang Juhua, Chen Xiaole

机构信息

School of Pharmacy, Department of Pharmacology, Fujian Medical University, Fuzhou, China.

Fujian Key Laboratory of Drug Target Discovery and Structural and Functional Research, School of Pharmacy, Fujian Medical University, Fuzhou, China.

出版信息

Front Pharmacol. 2021 May 13;12:681424. doi: 10.3389/fphar.2021.681424. eCollection 2021.

DOI:10.3389/fphar.2021.681424
PMID:34054555
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8155588/
Abstract

Diabetic nephropathy the main reason for end stage renal disease is a common microvascular complication in patients with type 1 and type 2 diabetes. The interleukin-6 (IL-6), acting as a pleiotropic cytokine, play key roles in main autoimmune disorders. The recombinant anti-IL-6R fusion proteins (VHH-0031) constructed and obtained in our lab is a dual target-directed single domain-based fusion protein against the interleukin-6 receptor. This study aims to explore the renoprotective effect of VHH-0031 in diabetic nephropathy. VHH-0031 treatment alleviated renal inflammation, morphologic injury and renal insufficiency in both Goto-Kakizaki rats and STZ-induced Sprague Dawley rats. These renoprotective effects of VHH-0031 are associated with alleviating inflammation and suppression of the JAK2/STAT3 signaling pathway. The mesangial cells treated with VHH-0031 exhibited anti-proliferation, anti-inflammation and inactivation of JAK2/STAT3 pathway under high glucose condition. In conclusion, this study demonstrates that VHH-0031 exhibited a potent protective effect in kidney of diabetic rats and its mechanism may be concerned with the inhibition of the IL-6R/JAK2/STAT3 pathway of glomerular mesangial cells.

摘要

糖尿病肾病是终末期肾病的主要原因，是1型和2型糖尿病患者常见的微血管并发症。白细胞介素-6（IL-6）作为一种多效性细胞因子，在主要自身免疫性疾病中起关键作用。我们实验室构建并获得的重组抗IL-6R融合蛋白（VHH-0031）是一种针对白细胞介素-6受体的双靶点单域融合蛋白。本研究旨在探讨VHH-0031在糖尿病肾病中的肾脏保护作用。VHH-0031治疗减轻了Goto-Kakizaki大鼠和链脲佐菌素诱导的Sprague Dawley大鼠的肾脏炎症、形态学损伤和肾功能不全。VHH-0031的这些肾脏保护作用与减轻炎症和抑制JAK2/STAT3信号通路有关。在高糖条件下，用VHH-0031处理的系膜细胞表现出抗增殖、抗炎和JAK2/STAT3通路失活。总之，本研究表明VHH-0031在糖尿病大鼠肾脏中表现出强大的保护作用，其机制可能与抑制肾小球系膜细胞的IL-6R/JAK2/STAT3通路有关。

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