Sufentanil enhances M1/M2 phenotypic polarization transition and alleviates LPS-triggered neuroinflammation in BV2 cells

To investigate the regulatory effects of Sufentanil (Suf) in BV2 cells stimulated with lipopolysaccharide (LPS). Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay, apoptosis was evaluated via flow cytometry, levels of inflammation factors were quantified using Enzyme-Linked Immunosorbent Assay (ELISA), pro-portions of cluster of differentiation (CD)206 and CD16/32 were determined through flow cytometry, and mRNA and protein expressions were analyzed using Reverse Transcription-quantitative Polymerase Chain Reaction (RT-qPCR) and western blot. Our findings demonstrate that Suf (10 µM and 20 µM) exerted no cytotoxic effects, and LPS stimulation of BV2 cells mimicked a neuropathic pain cell model. In addition, treatment using Suf enhanced cell viability and inhibited apoptosis in LPS-triggered BV2 cells, mitigated LPS-induced inflammation and promoted M1/M2 phenotypic polarization transition in BV2 cells, and attenuated the activation of the nuclear factor kappa-B (NF-κB) pathway induced by LPS treatment. In conclusion, Suf can enhance M1/M2 phenotypic polarization transition and attenuate LPS-mediated neuroinflammation in BV2 cells.