Pint aggravates renal injury induced by ischemia and reperfusion in rats via Nrf2/HO-1 mediated endoplasmic reticulum stress

被引:7
作者
Yu, Honglin [1 ]
Jiang, Guanjun [2 ]
Hu, Wei [3 ]
Xu, Changgeng [4 ]
机构
[1] Anhui Med Univ, Affiliated Hosp 1, Dept Radiol, Hefei, Anhui, Peoples R China
[2] Fifth Hosp Wuhan, Dept Urol, Wuhan, Peoples R China
[3] Univ South China, Hengyang Med Sch, Affiliated Hosp 1, Dept Androl, Hengyang, Hunan, Peoples R China
[4] Huazhong Univ Sci & Technol, Dept Urol, Cent Hosp Wuhan, Tongji Med Coll, Wuhan, Hubei, Peoples R China
关键词
NIMA-Interacting Peptdylproly1 Isomerase; Ischemia; Reperfuslon; NF-E2-Related Factor 2; Herne Oxygenase-1; Endoplasrnlc Reticulum Stress; OXIDATIVE STRESS; ISOMERIZATION; INHIBITION; APOPTOSIS; PROTECTS;
D O I
10.1590/acb370101
中图分类号
R61 [外科手术学];
学科分类号
摘要
Purpose: To investigate the role of peptidyl-prolyl cis/trans isomerase 1 (Pin1) on renal ischemia-reperfusion (I/R) injury and underlying mechanism.Methods: By establishing the in vitro and in vivo models of renal I/R, the role of Pin1 was explored by using molecular assays.Results: In renal I/R, endogenous Pin1 level was up-regulated in I/R-impaired kidney. Suppression of Pin1 with juglone afforded protection against I/R-mediated kidney dysfunction, and reduced I/R-induced endoplasmic reticulum (ER) stress in vivo. Consistent with the in vivo results, repression of Pin1 with juglone or gene knockdown with si-Pin1 conferred cytoprotection and restricted hypoxia/reoxygenation (H/R)-driven ER stress in HK-2 cells. Simultaneously, further study uncovered that Nrf-2/HO-1 signals was the association between Pin1 and ER stress in response to renal I/R. In addition, Nrf-2/HO-1 signal pathway was inactivated after kidney exposed to I/R, as indicated by the down-regulation of Nrf-2/HO-1 levels. Furthermore, inhibition of Pin1 remarkably rescued the inactivation ofNrf-2/HO-1.Conclusions:Pin1 modulated I/R-mediated kidney injury in ER stress manner dependent on Nrf2-HO-1 pathway in I/R injury.
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页数:11
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