| Objectives:To study the effect of hydrogen sulfide on ischemia-reperfusion injury(IR)in the rat liver and its mechanism.Methods: After constructing the model of hepatic ischemia-reperfusion injury through thehepatic artery ligation, then the model was divided into three groups:sham operationgroup(Sham group), ischemia-reperfusion injury group (IR group) and ischemic injury+hydrogen sulfide protection group (IR+NaHS group); The liver cell apoptosis in the threegroups were analyzed by using TUNEL situ staining and flow cytometry, as well asdetecting the cell injury indicator-ALT concentration. Real time-PCR, Western blots wereused to analyze the effect of exogenous hydrogen sulfide on the gene and proteinexpression of activating transcription factor6(ATF6) and CCAAT/enhancer-bindingprotein-homologous protein(CHOP), which were the key molecules of endoplasmicreticulum emergency (ERS) signaling pathway.Results:TUNEL in situ apoptosis and flow cytometry analysis showed that apoptosis in rathepatocytes of IR group was significantly increased,compared with the sham group(P<0.05). Compared with that of IR group(P<0.05),rat liver cell apoptosis of IR+NaHSgroup was significantly reduced; rat liver cell injury markers alanine aminotransferase（ALT）was increased significantly in IR group and sham group.But the serum ALT wasmarkedly decreased in IR+NaHS group,compared with the IR group,so the difference wasstatistically significant.Although it was increased significantly compared with that in thesham group, compared with that in IR+NaHS group, the ATF6and CHOP mRNA andprotein expression was significantly reduced(P<0.05).Conclusions:the model of hepatic ischemia reperfusion injury SD-rat was successfullyconstructed; hydrogen sulfide have a protective effect against ischemia reperfusion injuryby inhibiting the ATF6-CHOP gene expression, which were the critical signal molecule ofendoplasmic reticulum stress. |
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