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Published:
Jan 11, 2024Keywords:
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Main Article Content
ELAVL1 ameliorates sevoflurane induced neurotoxicity by inhibiting NLRP3 inflammasome activation
Abstract
Methods: A cell model was established in HT22 cells by exposing them to 3 % sevoflurane for 12 h. The HT22 cells were transfected with siRNA ELAVL1 (si-ELAVL1) or siRNA negative control (si-NC) to knockdown ELAVL1 expression. Enzyme-linked immunosorbent assay (ELISA) was performed to assess the levels of proinflammatory factors in HT22 cell culture supernatants. Cell apoptosis was analyzed using flow cytometry while apoptosis-related proteins and NLRP3 inflammasome pathway proteins were determined by western blot.
Results: ELAVL1 was upregulated in sevoflurane-exposed HT22 cells. Sevoflurane exposure also resulted in inflammation, apoptosis and activation of NLRP3 inflammasome of HT22 cells. Importantly, knockdown of ELAVL1 inhibited inflammation and apoptosis in HT22 cells caused by sevoflurane through the inhibition of IL-6, IL-1β and TNF-α production and bys regulating Bax and Bcl-2 protein expression. Furthermore, knockdown of ELAVL1 suppressed NLRP3 inflammasome activity as reflected by the inhibition of the expression of caspase 1, ASC, IL-1β and IL-18.
Conclusion: The findings of this study suggest that the knockdown of ELAVL1 alleviates the inflammation and apoptosis of HT22 cells induced by sevoflurane which impeded the activation of NLRP3 inflammasome, suggesting that ELAVL1 would make a good therapeutic target for sevoflurane-caused neurotoxicity.
