Effects of Ropivacaine Hydrochloride on the Expression of Type I Interferon and Its Receptor in SH-SY5Y Cells

Nerve injury caused by local anesthetics is a hot issue that people pay close attention to, and its mechanism has not been fully clarified. Type I interferon (I-IFN) is an important factor in regulating inflammatory response. In this study, SH-SY5Y cells were injured by ropivacaine hydrochloride in vitro. The cell viability, apoptosis rate, mRNA and protein expression of I-IFN and its receptor IFNAR, as well as the contents of inflammatory cytokines TNF-alpha, IL-6 and IL-10 were detected to explore the correlation between I-IFN and neurotoxicity induced by ropivacaine hydrochloride. The results showed that after treated with ropivacaine hydrochloride, the cell viability was decreased, the apoptosis rate was increased, the mRNA and protein expressions of IFN-alpha, IFN-beta, IFNAR1 and IFNAR2 were up-regulated, and the contents of inflammatory factors TNF-alpha, IL-6 and IL-10 were increased. These results suggest that type I interference and its receptor are associated with neurotoxicity of local anesthetics.