Role and Mechanism of NUP160

IF 0.8 4区医学 Q4 UROLOGY & NEPHROLOGY

Iranian journal of kidney diseases Pub Date : 2023-11-01

引用次数: 0

Abstract

\Introduction. Diabetes mellitus (DM) is one of the most common

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nup160调控的自噬在糖尿病肾病发病中的作用及机制

\介绍。糖尿病(DM)是世界范围内最常见的慢性疾病之一，糖尿病肾病(DN)是糖尿病最重要的并发症，发病率高，治疗难度大。本课题旨在探讨核孔蛋白160kDa (Nucleoporin 160kDa, NUP160)调控的自噬在DN发病中的作用及机制。方法:采用Western blot法检测糖尿病和非糖尿病患者肾脏组织中NUP160水平，分析NUP160与DN患者肾功能的关系。将足细胞分为标准组(培养基:标准葡萄糖溶液)、高糖(HG)组(HG溶液)、HG+si-NUP160组(HG溶液+si-NUP160转染)和HG+si-NC组(HG溶液+si-NUP160转染)四组，流式细胞术检测细胞凋亡，Western blot检测LC3B、prostacyclin_62 (P62)、Janus kinase 2 (JAK2)和Signal transductionand activator of transcription3 (STAT3)。结果:DN患者足细胞中NUP160降低，且与血尿素氮(BUN)、血清肌酐(Scr)、β2-微球蛋白(β2-MG)呈反比(P < 0.05)。与标准组比较，其他三组细胞凋亡率、P62水平、磷酸化-JAK2 (P -JAK2)/JAK2、磷酸化-STAT3 (P -STAT3)/STAT3、LC3B-Ⅱ/LC3B-Ⅰ比值均升高(P < 0.05)。HG+si-NUP160组细胞凋亡率、P62水平、P -JAK2/JAK2、P -STAT3/STAT3比值升高，LC3B-Ⅱ/LC3B-Ⅰ比值降低(P < 0.05)，而HG+si-NC组细胞凋亡率、P62水平、P -JAK2/JAK2、P -STAT3/STAT3比值降低(P < 0.05)，与HG组比较无明显变化(P > 0.05)。结论:NUP160在DN中下调，可通过激活JAK2/STAT3信号通路影响细胞自噬。DOI: 10.52547 / ijkd.7884。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Iranian journal of kidney diseases UROLOGY & NEPHROLOGY-

CiteScore

2.50

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： The Iranian Journal of Kidney Diseases (IJKD), a peer-reviewed journal in English, is the official publication of the Iranian Society of Nephrology. The aim of the IJKD is the worldwide reflection of the knowledge produced by the scientists and clinicians in nephrology. Published quarterly, the IJKD provides a new platform for advancement of the field. The journal’s objective is to serve as a focal point for debates and exchange of knowledge and experience among researchers in a global context. Original papers, case reports, and invited reviews on all aspects of the kidney diseases, hypertension, dialysis, and transplantation will be covered by the IJKD. Research on the basic science, clinical practice, and socio-economics of renal health are all welcomed by the editors of the journal.