Effect and mechanism of hyaluronic acid on the neurotoxic injury of lidocaine

Abstract

Hyaluronic acid (HA) is used to aid tissue repair and is a characterized inhibitor of TRPV1 channels. In this study, we investigated the effects of HA on lidocaine induced neurotoxicity and its mechanism of action. U87-MG cells with low (U87-MG-shTRPV1) or high (U87-MG-TRPV1) TRPV1 expression were studied. The control group was treated with lidocaine. The experimental group was treated with lidocaine and HA. Flow cytometry was used to assess the intracellular calcium concentration ([Ca2+] i) and cell apoptosis. Cell viability was detected by MTT assays. Compared to the control group, [Ca2+] i of U87-MG-TRPV1 and U87-MG cells were lower at T3, T4 and T5 (p < 0.05), apoptosis rates of U87-MG and U87-MG-TRPV1 cells were lower (p<0.05), and the cell viability of U87-MG and U87MG-TRPV1 cells were higher in the experimental group (p<0.05). HA reduces the toxic damage of lidocaine through blocking Ca2+ influx through TRPV1 channels, preventing Ca2+ overload, leading to nerve cell protection.