Effect of remifentanil on pain behavior in rats with sciatic nerve injury by regulating the IL-10/β-endorphin signaling pathway
Objective To investigate the effect of remifentanil on pain behavior in sciatic nerve injury(SNI)rats and the underlying mechanism.Methods The SNI rat model was established.Rats were randomly divided into sham operation group(cut open without SNI modeling),model group(SNI modeling),low-dose remifentanil group(5μg·kg-1·min-1),high-dose remifentanil group(20μg·kg-1·min-1)and remifentanil + inhibitor group(20μg·kg-1·min-1 remifentanil+ 10μL of anti-IL-10 antibody).The pain threshold and sciatic nerve index(SFI)of rats were evaluated.Masson staining was applied to evaluate target muscle atrophy.Enzyme-linked immunosorbent assay(ELISA)was applied to detect the levels of interleukin-1β(IL-1β),IL-6,and tumor necrosis factor-α(TNF-α).Immunofluorescence was applied to detect the positive expression of microtubule-associated protein 2(MAP2).Western blot was applied to detect the protein expressions of IL-10 and β-endorphin.Results Compared with those of the sham operation group,rats in the model group presented significantly lower pain threshold,SFI and protein expressions of IL-10 and β-endorphin,muscle atrophy,and significantly higher levels of IL-1β,IL-6 and TNF-α and protein expression of MAP2(P<0.05).Compared with those of model group,rats in the low-dose and high-dose remifentanil groups presented significantly higher pain threshold,SFI and protein expressions of IL-10 and β-endorphin,alleviated muscle atrophy,and significantly lower levels of IL-1β,IL-6 and TNF-α and protein expression of MAP2 in a dose-dependent manner(P<0.05).Compared with those of the high-dose remifentanil group,rats in the remifentanil + inhibitor group presented significantly lower pain threshold,SFI and protein expressions of IL-10 and β-endorphin,muscle atrophy,and significantly higher levels of IL-1β,IL-6 and TNF-α and protein expression of MAP2(P<0.05).Conclusion Remifentanil may inhibit pain behavior in SNI rats by activating the IL-10/β-endorphin signaling pathway.