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Published:
Apr 27, 2022DOI:
10.4314/tjpr.v21i2.7Keywords:
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Main Article Content
Eriocitrin alleviates sevoflurane-induced cytotoxicity in HT22 cells via Nrf2 pathway
Abstract
Purpose: To investigate the effect of eriocitrin on sevoflurane-induced neurotoxicity in mice.
Methods: Mouse hippocampal neurons (HT22) were exposed to different concentrations of sevoflurane for 6 h and then incubated with different concentrations of eriocitrin for another 24 h. Cell viability was determined by CCK8 assay, while fluorescence intensity of dichlorodihydrofluorescein was used to evaluate reactive oxygen species. Enzyme linked immunosorbent assay (ELISA) was used to determine oxidative stress, and cellular apoptosis was determined by flow cytometry.
Results: Sevoflurane exposure decreased HT22 cell viability, whereas incubation with eriocitrin increased viability of sevoflurane-treated HT22 cells (p < 0.05). Sevoflurane-induced increase in dichlorodihydrofluorescein fluorescence intensity was reduced by eriocitrin, but eriocitrin attenuated sevoflurane-induced increase in malondialdehyde, superoxide dismutase, and glutathione peroxidase in HT22 cells. Cell apoptosis increased after sevoflurane exposure, and eriocitrin suppressed apoptosis in sevoflurane-treated HT22 cells through downregulation of cleaved caspase-3 and cleaved caspase-9 (p< 0.05). Eriocitrin incubation enhanced protein expression of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H quinone dehydrogenase 1 (NQO1) in sevoflurane-treated HT22 cells (p < 0.05).
Conclusion: Eriocitrin ameliorates sevoflurane-induced oxidative stress and inflammatory response in HT22 cells via activation of Nrf2/HO-1/NQO1 signaling. Thus, agent may be useful in the treatment of sevoflurane-induced toxicity, but in vivo studies are required to buttress this.
