Abstract
Objective To investigate the role of extracellular signal-regulated kinase 1/2(ERK1/2) in attenuation of hepatic ischemia/reperfusion injury by dexmedetomidine (Dex) preconditioning in rats. Methods Adult male SD rats were randomly allocated into four groups (n=6): Sham group (group S), hepatic ischemia/reperfusion injury(HI/RI) group (group HI/RI), Dex pretreatment in HI/RI group (group D), U0126 (MEK inhibitor) pretreatment followed by same treatments as D group (group U). The results were observed at 6 h of reperfusion. The effects of Dex on phosphorylate(p)-ERK1/2 expression in the ischemic liver were measured by immunohistochemistry. Hepatic injuries were evaluated with the activity of ALT and AST, levels of Cleaved caspase-3, TUNEL assay, and H-E staining. Results Compared with group HI/RI, group D exhibited reduce activity of ALT and AST, lower levels of Cleaved casepase-3, and attenuated apoptosis index(P<0.05), but elevated levels of p-ERK1/2 (P<0.05). Compared with group D, group U showed enhanced activity in ALT and AST, raised expression of Cleaved casepase-3, increased apoptosis index (P<0.05), but reduced, expression of p-ERK1/2(P<0.05). Conclusions Dex treatment reduced expression of casepase-3 and inflammation in HI/RI rats, probably through activationg the ERK1/2 pathway. Key words: Dexmedetomidine; Ischemia/reperfusion injury; Liver; Extracellular signal-regulated kinase 1/2; Apoptosis
Published Version
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