Sodium Ferulate Attenuates Oxidative Stress Induced Inflammation via Suppressing NALP3 Inflammasome and p38 MAPK Signal Pathway

OBJECTIVE:To investigate the changes of NACHT-PYD-containing protein 3(NALP3) inflammasome and p38 mitogen-activated protein kinase (MARK),and the interventional mechanism of sodium ferulate (SF) in mouse embryonic fibroblasts (NIH-3T3 cells) under oxidative stress. METHODS:NIH-3T3 cells cultured in vitro were divided into 6 groups,including control group,H₂O₂ stress group (H₂O₂ 200 μmol/L),SF group (SF 400 μg/mL),antioxidant group (H₂O₂ 200 μmol/L+NAC 5 mmol/L),p38 MAPK blockers group (H₂O₂ 200 μmol/L+SB203580 5 μmol/L),H₂O₂+SF group (H₂O₂ 200 μmol/L+SF 400 μg/mL). The mRNA expression levels of NALP3, Caspase-1 and p38α were evaluated by fluorescent quantitative real-time PCR (qRT-PCR) at 24 h after cell culture; Western blot was performed to detect the expressions of NALP3,p-p38 to p38 protein (the activation of p38 MAPK signaling pathway expressed by the ratio of p-p38 to p38) at 48 h after cell culture; The levels of interleukin-1beta (IL-1β) in different groups were detected by ELISA at 2 h after cell culture. RESULTS:Compared with control group,H₂O₂ could not only increase the expression levels of NALP3, Caspase-1,p38α mRNAs and NALP3,p-p38/p38 proteins but also the secretion of IL-1β in NIH-3T3 cells when compared with the control group (P 0.05). CONCLUSION:The mechanism of sodium ferulate attenuated oxidative stress induced inflammation may be through blunting p38 MAPK signal pathway,the expression of NALP3 inflammasome,Caspase-1 and the secretion of IL-1β are reduced.