Kapsaisin apoptozu düzenleyerek SH-SY5Y hücrelerinde bupivakain anestezisinin neden olduğu nörotoksisiteyi hafifletmektedir

Abstract

Objective: Bupivacaine administered for local anesthesia can cause critical neurotoxicity and neurological dysfunctions. Any substance that can reduce bupivacaine-mediated toxic effects will be of great interest during surgical procedures and in the pain management process. In this context, we evaluated capsaicin, an alkaloid of Capsicum annuum (cayenne pepper), which has been intensively researched for its neuroprotective effect due to its various biological effects such as cardioprotective, antiinflammatory, analgesic, thermogenic, and benefits on the gastrointestinal tract. Methods: In this study, we researched the in vitro effect of capsaicin in SH-SY5Y cells with a model of bupivacaine-mediated neurotoxicity. Cell proliferation assay was handled by XTT, and apoptosis was determined by flow cytometry analysis. Results: We observed a notable increase in apoptosis induction with a significant decrease in the viability of cells exposed to bupivacaine at 1 mM. We found that bupivacaine-mediated cytotoxicity was reduced when increasing concentrations of capsaicin were applied to bupivacaine-treated cells. At the same time, capsaicin also reduced apoptosis in SH-SY5Y cells exposed to bupivacaine. Conclusion: According to our results, it is thought that the administration of capsaicin against bupivacaine-mediated neurotoxicity may be an alternative neuroprotective agent by suppressing the apoptosis response in neurons.