Effect of remifentanil on retinal ischemia-reperfusion injury in mice by regulating the JAK2/STAT3 signal-ing pathway
Objective To investigate the effect of remifentanil(RFTN)on retinal ischemia-reperfusion(RIRI)injury in mice by regulating the JAK2/STAT3 signaling pathway.Methods The mice were separated into Sham group,Model group,RFTN-L low-dose group,RFTN-H high-dose group,and RFTN-H+Colivelin group(JAK2 activator).HE staining was applied to observe the retinal morphology of mice in each group.TUNEL staining method was applied to detect apoptosis in retinal tissue cells.ELISA method was applied to detect the levels of TNF-α,IL-10,and IL-1β in mouse retinal tissue.The commercialized reagent kits were applied to detect the levels of SOD,MDA,and CAT in mouse retinal tissue.Western blot was applied to detect the expression levels of NLRP3,caspase-1,JAK2,STAT3,and cleaved caspase-3 proteins in retinal tissue.Results Compared with the Sham group,the retinal tissue of mice in the Model group showed obvious damage,the thickness of GCL,the number of RGCs,apoptosis rate of retinal tissue cells,levels of TNF-α and IL-1β,content of MDA,the expression levels of NLRP3,caspase-1,cleaved caspase-3,p-JAK2/JAK2,p-STAT3/STAT3 proteins were obviously increased,the lev-el of IL-10,activities of SOD,and CAT in retinal tissue were obviously reduced(P＜0.05).Compared with the Mod-el group,the retinal tissue damage of mice in the RFTN-L and RFTN-H groups was obviously reduced,the thick-ness of GCL,the number of RGCs,apoptosis rate of retinal tissue cells,levels of TNF-α and IL-1β,content of MDA,the expression levels of NLRP3,caspase-1,cleaved caspase-3,p-JAK2/JAK2,p-STAT3/STAT3 proteins were obviously reduced,the level of IL-10,activities of SOD,and CAT in retinal tissue were obviously increased(P＜0.05).Colivelin could weaken the protective effect of RFTN on RIRI mice(P＜0.05).Conclusion RFTN can re-duce inflammation,oxidative stress,and retinal tissue cell apoptosis in RIRI mice,alleviate retinal damage,and may be related to the inhibition of the JAK2/STAT3 signaling pathway.
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