Abstract
Ropivacaine is a commonly used local anesthetic in the clinic due to its low toxicity to the cardiovascular system or central nervous system, good tolerance and high clearance rate. The present study intended to investigate the effect of ropivacaine on PM2.5-induced acute lung injury (ALI) and reveal the underlying mechanism. After ropivacaine exposure, cell viability, oxidative stress and inflammation in PM2.5-induced BEAS-2B cells were assessed by Cell Counting Kit-8 and DCFH-DA staining, corresponding commercial kits and ELISA, respectively. The effects of ropivacaine on the expression of MMP9 and MMP12 and the proteins related to NLRP3/Caspase-1 signaling were then determined by western blot and reverse transcription-quantitative PCR analyses. In addition, NLR family pyrin domain containing 3 (NLRP3) agonist monosodium urate (MSU) was used to treat BEAS-2B cells followed by ropivacaine treatment and the effects on the above-mentioned cellular behaviors were determined again. The results indicated that the viability of BEAS-2B cells was decreased after PM2.5 induction, accompanied by aggravated oxidative stress and inflammation. However, ropivacaine alleviated oxidative stress and inflammation in PM2.5-induced BEAS-2B cells in a dose-dependent manner. Ropivacaine was also indicated to decrease the expression levels of NLRP3/Caspase-1 signaling-related proteins in PM2.5-induced BEAS-2B cells. Furthermore, cell viability was decreased, while oxidative stress and inflammatory response were aggravated, in PM2.5-induced BEAS-2B cells treated with MSU. In summary, the present results implied that ropivacaine exerted protective effects on PM2.5-induced ALI, and this effect may be related to NLRP3/Caspase-1 signaling.