Nanjing Medical University, Nanjing, Jiangsu, P.R. China.
Eur Rev Med Pharmacol Sci. 2020 Jun;24(12):7092-7100. doi: 10.26355/eurrev_202006_21703.
To explore the protective effect of curcumin on lidocaine-insulted PC12 cells.
We first treated PC12 cells with different doses of lidocaine, and then treated the cells with curcumin or Nod-like receptor pyrin domain3 (NLRP3) inhibitor (MCC950). Subsequently, the cell viability, apoptosis, reactive oxygen species (ROS) production and NLRP3 inflammasome were detected by cell counting kit-8 (CCK8), Annexin V/PI staining, FCM and Western blot analysis, respectively, and the level of IL-1β in PC12 cells was determined by an enzyme-linked immunosorbent assay (ELISA) kit.
Lidocaine inhibited the viability of PC12 cells, and it induced cell apoptosis, promoted ROS release and activated NLRP3 inflammasome in PC12 cells, but its effects were reversed by the treatment of curcumin. Moreover, NLRP3 over-expression also induced cytotoxicity in PC12 cells, which was also rescued by the treatment of curcumin.
Our study indicates that curcumin exerts protective effect against lidocaine-induced cytotoxicity on PC12 cells by suppressing the activity of NLRP3 inflammasome, which provides new ideas on screening natural product for neurological damage therapy.
探讨姜黄素对利多卡因损伤的 PC12 细胞的保护作用。
首先用不同剂量的利多卡因处理 PC12 细胞,然后用姜黄素或 Nod 样受体含pyrin 结构域 3(NLRP3)抑制剂(MCC950)处理细胞。随后,通过细胞计数试剂盒-8(CCK8)、Annexin V/PI 染色、FCM 和 Western blot 分析分别检测细胞活力、细胞凋亡、活性氧(ROS)产生和 NLRP3 炎性体,并用酶联免疫吸附试验(ELISA)试剂盒检测 PC12 细胞中 IL-1β 的水平。
利多卡因抑制 PC12 细胞活力,并诱导 PC12 细胞凋亡,促进 ROS 释放和激活 NLRP3 炎性体,但姜黄素处理可逆转其作用。此外,NLRP3 过表达也诱导 PC12 细胞的细胞毒性,而姜黄素处理可挽救这一作用。
本研究表明,姜黄素通过抑制 NLRP3 炎性体的活性对利多卡因诱导的 PC12 细胞毒性发挥保护作用,为筛选治疗神经损伤的天然产物提供了新的思路。