ArticleIn vitro cellular & developmental biology. Animal2024
Inhibition of FOXO3 ameliorates ropivacaine-induced nerve cell damage through the miR-126-5p/TRAF6 axis.
Article in In vitro cellular & developmental biology. Animal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Local anesthetics, such as ropivacaine (Ropi), are toxic to nerve cells. We aimed to explore the role of forkhead box O3 (FOXO3) in Ropi-induced nerve injury to provide a theoretical basis for reducing the anesthetic neurotoxicity. SK-N-SH cells were cultured and treated with different concentrations of Ropi. Cell viability, apoptosis, cytotoxicity (LDH/ROS/SOD), and levels of FOXO3, miR-126-5p, and tumor necrosis factor receptor-associated factor 6 (TRAF6) were detected. The enrichment of FOXO3 on the miR-126-5p promoter was analyzed. The binding relationships among FOXO3, miR-126-5p promoter sequence, and TRAF6 3'UTR sequence were verified. Combined experiments detected the regulatory role of FOXO3/miR-126-5p/TRAF6 in Ropi-induced nerve injury. FOXO3 was upregulated in Ropi-induced nerve cell damage. Inhibition of FOXO3 ameliorated Ropi-induced decreased cell viability, and increased apoptosis and cytotoxicity. FOXO3 bound to the miR-126-5p promoter and inhibited its expression, thereby counteracting miR-126-5p-induced repression. miR-126-5p inhibition and TRAF6 overexpression partially reversed the alleviative effect of FOXO3 inhibition on Ropi-induced nerve cell damage. In conclusion, FOXO3 aggravated the neurotoxicity of Ropi through miR-126-5p downregulation and TRAF6 upregulation, suggesting that FOXO3 inhibitor could be an adjuvant agent for local anesthetics, to alleviate local anesthetics-induced neurotoxicity.
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