摘要
BACKGROUND:Ischemic preconditioning(IPC) is a strategy to reduce ischemia-reperfusion(I/R) injury.The protective effect of remote ischemic preconditioning(RIPC) on liver I/R injury is not clear.This study aimed to investigate the roles of RIPC in liver I/R in fatty liver rats and the involvement of endothelial nitric oxide synthase-nitric oxide(eNOS-NO) pathway and microRNA expressions in this process.METHODS:A total of 32 fatty rats were randomly divided into the sham group,I/R group,RIPC group and RIPC+I/R group.Serum alanine aminotransferase(ALT),aspartate aminotransferase(AST) and nitric oxide(NO) were measured.Hematoxylin-eosin staining was used to observe histological changes of liver tissues,TUNEL to detect hepatocyte apoptosis,and immunohistochemistry assay to detect heat shock protein 70(HSP70) expression.Western blotting was used to detect liver inducibleNOS(iNOS) and eNOS protein levels and realtime quantitative polymerase chain reaction to detect miR-34a,miR-122 and miR-27b expressions.RESULTS:Compared with the sham and RIPC groups,serum ALT,AST and iNOS in liver tissue were significantly higher in other two groups,while serum NO and eNOS in liver tissue were lower,and varying degrees of edema,degeneration and inflammatory cell infiltration were found.Cell apoptosis number was slightly lower in the RIPC+I/R group than that in I/R group.Compared with the sham group,HSP70 expressions were significantly increased in other three groups(all P<0.05).Compared with the sham and RIPC groups,elevated miR-34a expressions were found in I/R and RIPC+I/R groups(P<0.05).MiR-122 and miR-27b were found significantly decreased in I/R and RIPC+I/R groups compared with the sham and RIPC groups(all P<0.05).CONCLUSION:RIPC can reduce fatty liver I/R injury by affecting the eNOS-NO pathway and liver microRNA expressions.
BACKGROUND: Ischemic preconditioning (IPC) is a strategy to reduce ischemia-reperfusion (I/R) injury. The protective effect of remote ischemic preconditioning (RIPC) on liver I/R injury is not clear. This study aimed to investigate the roles of RIPC in liver I/R in fatty liver rats and the involvement of endothelial nitric oxide synthase-nitric oxide (eNOS-NO) pathway and microRNA expressions in this process. METHODS: A total of 32 fatty rats were randomly divided into the sham group, I/R group, RIPC group and RIPC+I/R group. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and nitric oxide (NO) were measured. Hematoxylin-eosin staining was used to observe histological changes of liver tissues, TUNEL to detect hepatocyte apoptosis, and immunohistochemistry assay to detect heat shock protein 70 (HSP70) expression. Western blotting was used to detect liver inducible NOS (iNOS) and eNOS protein levels and realtime quantitative polymerase chain reaction to detect miR-34a, miR-122 and miR-27b expressions. RESULTS: Compared with the sham and RIPC groups, serum ALT, AST and iNOS in liver tissue were significantly higher in other two groups, while serum NO and eNOS in liver tissue were lower, and varying degrees of edema, degeneration and inflammatory cell infiltration were found. Cell apoptosis number was slightly lower in the RIPC+I/R group than that in I/R group. Compared with the sham group, HSP70 expressions were significantly increased in other three groups (all P<0.05). Compared with the sham and RIPC groups, elevated miR-34a expressions were found in I/R and RIPC+I/R groups (P<0.05). MiR-122 and miR-27b were found significantly decreased in I/R and RIPC+I/R groups compared with the sham and RIPC groups (all P<0.05). CONCLUSION: RIPC can reduce fatty liver I/R injury by affecting the eNOS-NO pathway and liver microRNA expressions.
基金
supported by a grant from 2013 Applied Basic Research of Changzhou Bureau of Science and Technology(CJ20130044)
关键词
FATTY
IPC
fatty liver
ischemia-reperfusion
remote ischemic preconditioning
nitric oxide
heat shock protein 70
endothelial nitric oxide synthase
inducible nitric oxide synthase
liver microRNA
