Tilting the balance of tubular cell fate toward survival contributes to ischemic tolerance in kidney
10.3760/cma.j.issn.1001-7097.2011.03.015
- VernacularTitle:通过短时间预缺血改变肾小管上皮细胞命运诱导肾脏缺血耐受
- Author:
Suhua JIANG
;
Jianzhou ZOU
;
Hong LIU
;
Li REN
;
Xunhui XU
;
Yue CHEN
;
Xiaoqiang DING
- Publication Type:Journal Article
- Keywords:
Reperfusion injury;
Kidney tubules;
Epithelial cells;
Cell proliferation;
Ischemic tolerance;
Necrosis;
Apoptosis
- From:
Chinese Journal of Nephrology
2011;27(3):198-202
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role of brief ischemia pretreatment in the induction of renal ischemic tolerance,and investigate its effects on tubular cell necrosis,apoptosis and proliferation. Methods Male Sprague-Dawley rats were randomly divided into three groups,including sham-operated group (Sham),ischemia/reperfusion injured group subjected to theocclusion of both renal pedicles for 40 min followed by reperfusion(I/R),and preconditioned group with 20-min ischemia pretreatment induced 4 days before I/R(IPC).Histological changes were evaluated by PAS staining.The ultra-structure of tubular cells was observed by transmission electron microscopy(TEM).Apoptosis was confirmed by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL).The proliferation of tubular cells was evaluated with proliferating cell nuclear antigen(PCNA). Results Twenty-minites ischemia pretreatment offered both promising functional and histological protection against 40-min ischemia/reperfusion injury (P<0.01).The mortality rate wag reduced from 33%in I/R group to 0 in IPC group.The renopmtection offered by 20-min ischemia pretreatment was accompanied with reduced postischemic tubular cell apoptosis and necrosis (P<0.05), and increased cell proliferation (PCNA positive) (P< 0.01). Conclusions Brief and sublethal prior ischemia can render the kidney more tolerant to subsequent prolonged I/R injury. Its ability to tilt the balance of tubular cell fate toward survival, reducing postischemic cell death and enhancing cell proliferation, may play an important role in renal protection of ischemic preconditioning.
