Effects and underlying mechanisms of Cyr61 overexpression on cell apoptosis in early stage of ischemic acute kidney injury
10.3760/cma.j.issn.1001-7097.2016.07.006
- VernacularTitle:Cyr61过表达对缺血性急性肾损伤早期细胞凋亡的影响
- Author:
Yan XU
;
Wei JIANG
;
Rui MA
;
Ruixia MA
;
Xuemei LIU
- Publication Type:Journal Article
- Keywords:
Renal tubular necrosis,acute;
Cell apoptosis;
Tumor necrosis factor-alpha;
Cyr61;
Receptors,tumor necrosis factor,typeⅠ
- From:
Chinese Journal of Nephrology
2016;32(7):513-518
- CountryChina
- Language:Chinese
-
Abstract:
Objective To detect the effect and mechanism of Cyr61 on the apoptosis of renal tissue caused by early stage of ischemic acute kidney injury (AKI). Methods 30 SD rats were randomized into 5 groups, including control group, AKI group, AKI+bicarbonate group, AKI+blank virus group, and AKI+over?expression Cyr61 virus group. After animal models were created for 2h, serum and renal tissue were collected from sacrificed animals. Expression level of TNF?α was determined by ELISA. HE staining was used to observe the histologic changes of renal tissues. The levels of NF?κB p65 and TNFR1 were measured by immunohistochemical method. RT?PCR and Western blotting assay were adopted to detect the mRNA and protein expression levels of NF?κB p65, TNFR1 and Caspase3. Results Compared with control group, AKI group, AKI+bicarbonate group, AKI+blank virus group, AKI+over?expression Cyr61 virus group had obvious kidney injury. The levels of TNF?α, the mRNA and protein expression levels of NF?κB p65, TNFR1 and caspase3 were markedly up?regulated. Over?expression of Cyr61 significantly attenuated the degree of pathological injury, numbers of apoptotic renal tubular epithelial cells and increased the degree of Scr. Although compared with other groups, the level of TNF?α in kidney tissue had no difference, there was obvious decreased protein level of NF?κB p65, while the increase of TNFR1 and Caspase3 protein was moderate. Conclusions During the early stage of AKI, over expression of Cyr61 could inhibit apoptosis, which may be related to the suppression of TNFR1 transcriptional expression and interference of TNF?αpathway. Its underlying mechanism therefore deserves further research.
