Hydrogen Sulfide Inhibits High-Salt Diet-Induced Renal Oxidative Stress and Kidney Injury in Dahl Rats.
Hydrogen Sulfide Inhibits High-Salt Diet-Induced Renal Oxidative Stress and Kidney Injury in Dahl Rats.
复制标题
硫化氢抑制 Dahl 大鼠高盐饮食引起的肾氧化应激和肾损伤
DOI：
10.1155/2016/2807490
复制
发表时间：
2016
影响因子：
--
通讯作者：
Jin H
中科院分区：
文献类型：
--
作者：
Huang P;Shen Z;Liu J;Huang Y;Chen S;Yu W;Wang S;Ren Y;Li X;Tang C;Du J;Jin H
背景本研究旨在探讨硫化氢是否能抑制高盐饮食诱导的Dahl大鼠肾脏过度氧化应激和肾损伤。方法.使用雄性盐敏感性Dahl和SD大鼠。测量血压、血肌酐、尿素、肌酐清除率和24小时尿蛋白定量。观察肾脏超微结构变化。检测肾组织I、III型胶原含量、氧化剂和抗氧化剂水平。检测到Keap 1/Nrf 2缔合和Keap 1 s-硫水合。结果高盐饮食8周后，Dahl大鼠血压明显升高，肾功能和结构受损，肾组织胶原沉积增多，肾组织MPO活性、H2 O2、MDA、GSSG和·OH含量增加，肾组织T-AOC和GSH含量、CAT、GSH-PX和SOD活性及SOD表达降低。此外，Dahl大鼠肾组织中内源性H2S减少。H_2S供者可降低血压，改善肾功能和结构，抑制肾组织胶原过度沉积，增强肾组织抗氧化能力，减轻肾组织氧化应激。H2S通过诱导Keap 1 s-硫水合和随后的Keap 1/Nrf 2解离来激活Nrf 2。结论. H2S保护高盐饮食引起的肾损伤，与增强抗氧化能力和抑制肾氧化应激有关。
Background. The study was designed to investigate if H2S could inhibit high-salt diet-induced renal excessive oxidative stress and kidney injury in Dahl rats. Methods. Male salt-sensitive Dahl and SD rats were used. Blood pressure (BP), serum creatinine, urea, creatinine clearance rate, and 24-hour urine protein were measured. Renal ultra- and microstructures were observed. Collagen-I and -III contents the oxidants and antioxidants levels in renal tissue were detected. Keap1/Nrf2 association and Keap1 s-sulfhydration were detected. Results. After 8 weeks of high-salt diet, BP was significantly increased, renal function and structure were impaired, and collagen deposition was abundant in renal tissues with increased renal MPO activity, H2O2, MDA, GSSG, and •OH contents, reduced renal T-AOC and GSH contents, CAT, GSH-PX and SOD activity, and SOD expressions in Dahl rats. Furthermore, endogenous H2S in renal tissues was decreased in Dahl rats. H2S donor, however, decreased BP, improved renal function and structure, and inhibited collagen excessive deposition in kidney, in association with increased antioxidative activity and reduced oxidative stress in renal tissues. H2S activated Nrf2 by inducing Keap1 s-sulfhydration and subsequent Keap1/Nrf2 disassociation. Conclusions. H2S protected against high-salt diet-induced renal injury associated with enhanced antioxidant capacity and inhibited renal oxidative stress.