RIP3 expression and function in the liver of rats following ischemic postconditioning
10.3969/j.issn.1009-9905.2017.01.002
- VernacularTitle:RIP3在大鼠肝脏缺血后处理中的表达与作用
- Author:
Wei XIE
;
Dajin LIU
;
Xi LI
;
Zhaohui ZHANG
;
Wancheng NIU
;
Hongzun CUI
;
Feng ZHOU
- Keywords:
Ischemic reperfusion injury;
Ischemic postconditioning;
Liver damage;
Necroptosis;
RIP3
- From:
Chinese Journal of Current Advances in General Surgery
2017;20(1):5-9
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression and function of RIP3 in the liver of rats following ischemic postconditioning.Methods:The model of 70% hepatic ischemia and reperfusion was established,then a total of forty healthy adult male Sprague-Dawley(SD) rats were divided randomly into four groups,ten rats in each group:a sham-operation group (Sham group);an ischemia reperfusion injury group(IR group);an ischemic postconditioning group(IPO group);an ischemic postconditioning and necrostatin-1 group (Nec-1 group).The blood samples and liver tissues were collected.The serum levels of ALT and AST were detected,and the liver histological examination was performed.Western-bolt was used to detect the TNF-α and RIP3 levels.Results:Compared with the IR group,ALT and AST in serum were significantly declined in the IPO group (P<0.05);The liver damage after ischemia and reperfusion was improved obviously in the IPO group compared to which in the IR group;The Suzuki's scores was increased in the IR group compared to which in the IPO group (P<0.05);There was a low grade of TNF-α and RIP3 in the Sham group,whereas the level of TNF-α and RIP3 significantly increased in the IR and IPO and Nec-1 group(P<0.05);Compared with the IR group,the level of RIP3 was further decreased in the IPO group (P<0.05);Compared with the IPO group,the level of RIP3 was further decreased in the Nec-1 group (P<0.05).Conclusion:RIP3-mediated necroptosis was involved during hepatic ischemia postconditioning,and the protective effect of ischemia postconditioning may act as reducing necroptosis by cutting down the levels of RIP3.