The Effect of Moringa Isothiocyanate-1 on Renal Damage in Diabetic Nephropathy.

IF 0.8 4区 医学 Q4 UROLOGY & NEPHROLOGY
Iranian journal of kidney diseases Pub Date : 2023-09-01
Lijing Chen, Deyong Fan, Fei Guo, Jiuhong Deng, Linlin Fu
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引用次数: 0

Abstract

Introduction: Diabetic nephropathy (DN) is the most common clinical complication of diabetes mellitus. Moringa isothiocyanate-1 (MIC-1) is effective in the treatment of diabetes mellitus, but its mechanism of action in DN remains obscure. This research specifically probed the role of MIC-1 in modulating renal injury in DN.

Methods: Six db/m mice were assigned to control group and twelve db/db mice were randomly allocated to the db/db and db/db + MIC-1 groups. The body and kidney weights of the mice were monitored. Renal function indicators and oxidative stress-related markers were assessed by automatic biochemical analyzer and ELISA method. The pathological changes, apoptosis of renal tissues, extracellular regulated protein kinases (ERK) 1/2/ Nuclear factor erythroid2-related factor 2 (Nrf2) pathway-related markers, and the positive expressions of podocalyxin (Pod) and synaptopodin (Syn) were measured by H&E, PAS, and TUNEL staining, Western blot, and IHC assay.

Results: MIC-1 reduced the body and kidney weights, and increased the kidney organ index (calculated as 100*kidney weight/ body weight) in db/db mice. In addition, MIC-1 improved renal function, kidney tissue injury, and apoptosis of db/db mice. MIC1 noticeably repressed the contents of reactive oxygen species (ROS) and malondialdehyde (MDA) and enhanced the contents of (glutathione) GSH, superoxide dismutase (SOD), and catalase (CAT) in db/db mice. At molecular level, db/db mice showed a decrease in p-ERK/ERK, Nrf2, SOD-1, heme oxygenase 1 (HO-1), and CAT and an increase in p- inhibitor kappa B alpha (IKBα) and p-Nuclear factor-kappa B (P65/P65), which were reversed when MIC-1 was administered. Furthermore, MIC-1 facilitated the positive expressions of Pod and Syn of the kidney tissues in db/db mice.

Conclusion: MIC-1 reduces oxidative stress and renal injury by activating the ERK/Nrf2/HO-1 signaling and repressing the NFκB signaling in db/db mice.  DOI: 10.52547/ijkd.7515.

辣木异硫氰酸盐-1对糖尿病肾病肾损伤的影响。
引言:糖尿病肾病(DN)是糖尿病最常见的临床并发症。辣木异硫氰酸酯-1(MIC-1)对治疗糖尿病有效,但其在DN中的作用机制尚不清楚。方法:将6只db/m小鼠分为对照组,12只db/db小鼠随机分为db/db组和db/db+MIC-1组。监测小鼠的身体和肾脏重量。采用全自动生化分析仪和ELISA法对肾功能指标和氧化应激相关标志物进行评估。通过H&E、PAS、TUNEL染色、Western blot和IHC检测肾组织的病理变化、细胞外调节蛋白激酶(ERK)1/2/核因子-红细胞2型相关因子2(Nrf2)通路相关标志物以及足角蛋白(Pod)和突触蛋白(Syn)的阳性表达。结果:MIC-1降低了db/db小鼠的体重和肾重,并增加了肾器官指数(按100*肾重/体重计算)。此外,MIC-1改善了db/db小鼠的肾功能、肾组织损伤和细胞凋亡。MIC1显著抑制db/db小鼠的活性氧(ROS)和丙二醛(MDA)含量,并提高谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)含量。在分子水平上,db/db小鼠表现出p-ERK/ERK、Nrf2、SOD-1、血红素加氧酶1(HO-1)和CAT的减少,以及p-抑制剂κBα(IKBα)和p-核因子κB(P65/P65)的增加,当给予MIC-1时,这一现象逆转。此外,MIC-1促进db/db小鼠肾组织Pod和Syn的阳性表达。结论:MIC-1通过激活db/db小鼠ERK/Nrf2/HO-1信号传导和抑制NFκB信号传导,减轻氧化应激和肾损伤。DOI:10.52547/ijkd.7515。
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
Iranian journal of kidney diseases UROLOGY & NEPHROLOGY-
CiteScore
2.50
自引率
0.00%
发文量
43
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.
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