Eriocitrin alleviates sevoflurane-induced cytotoxicity in HT22 cells via Nrf2 pathway

Purpose: To investigate the effect of eriocitrin on sevoflurane-induced neurotoxicity in mice.Methods: Mouse hippocampal neurons (HT22) were exposed to different concentrations sevoflurane for 6 h and then incubated with another 24 h. Cell viability was determined by CCK8 assay, while fluorescence intensity dichlorodihydrofluorescein used evaluate reactive oxygen species. Enzyme linked immunosorbent assay (ELISA) determine oxidative stress, cellular apoptosis flow cytometry.Results: Sevoflurane exposure decreased HT22 cell viability, whereas incubation increased sevoflurane-treated cells (p < 0.05). Sevoflurane-induced increase reduced eriocitrin, but attenuated malondialdehyde, superoxide dismutase, glutathione peroxidase cells. after exposure, suppressed through downregulation cleaved caspase-3 caspase-9 (p< Eriocitrin enhanced protein expression nuclear factor E2-related 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1) 0.05).Conclusion: ameliorates stress inflammatory response via activation Nrf2/HO-1/NQO1 signaling. Thus, agent may be useful treatment toxicity, vivo studies are required buttress this.