Protective mechanism of ischemic preconditioning on apoptosis induced by kidney ischemia - reperfusion
10.3760/cma.j.issn.2095-428X.2016.05.009
- VernacularTitle:缺血预处理对大鼠缺血再灌注肾损伤诱发凋亡的保护机制
- Author:
Ying WANG
;
Zhihui LI
;
Xu DENG
;
Zhijuan KANG
;
Tuanhong XIA
;
Yan YIN
- Publication Type:Journal Article
- Keywords:
Ischemia - reperfusion injury;
Acute kidney injury;
Ischemic preconditioning;
Bax;
Bcl - 2;
Apoptosis
- From:
Chinese Journal of Applied Clinical Pediatrics
2016;31(5):354-358
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of ischemia preconditioning(IPC)on apoptosis in-duced by renal ischemia - reperfusion(IR)and relations to the changing expressions of Bcl - 2,Bax in rat kidney. Methods Ischemia models were induced by clipping bilateral renal pedicles for 30 min by using the artery clamp;IPC group was induced by clipping bilateral renal pedicles for 15 min,4 days later IR was performed again by clipping bila-teral renal pedicle for 30 min. Rats were randomly divided into 5 groups with 5 animals in each group:control group(C group),sham - operation group(S group),IR group,IPC group(IPC ﹢ IR group),sham IPC group(S ﹢ IR group),all groups were randomly divided into 9 sub groups(0 h,3 h,6 h,12 h,24 h,48 h,3 d,5 d,7 d)except C group according to the time points after reperfusion. Occurrence of apoptosis was detected by terminal deoxynuleotidyl transferase media-ted dUTP nick end and labeling(TUNEL)method;the mRNA expression and protein levels of Bax and Bcl - 2 were de-tected by reverse transcriptase - polymerase chain reaction and quantitave immunohistochemisty. Results (1)Com-pared with S group and S ﹢ IR group,serum creatinine,blood urea nitrogen,kidney pathological damage scores in IR group gradually increased after IR,and peak point was 24 h after reperfusion;among all the subgroups there was a sig-nificant difference(all P ﹤ 0. 01). The expression of Bax,Bcl - 2 mRNA raised sharply in IR group after reperfusion, peaking at 6 h,24 h of reperfusion respectively,2. 66 ± 0. 12,2. 70 ± 0. 10,and among all the subgroups there was a sig-nificant difference(all P ﹤ 0. 01);the expression of Bax,Bcl - 2 protein had significant difference(all P ﹤ 0. 05). TUNEL immunofluorescence staining showed C group and S group had no obvious apoptosis cells in renal tubular epi-thelium;epithelial cell apoptosis after IR gradually increased in IR group,peaking at 24 h of reperfusion[(25. 07 ± 2. 29)% ].(2)Compared with IR group and S ﹢ IR group,pathological injury was significantly decreased in IPC ﹢ IR group;the expression of Bax,Bcl - 2 mRNA and protein,apoptosis cells were significantly decreased in IPC ﹢ IR group (all P ﹤ 0. 05). Conclusions Bax,Bcl - 2 are closely associated with kidney injury induced by IR. IPC may regulate acute kidney injuries by regulating Bax/ Bcl - 2.
