Oleanic acid inhibits LPS-induced inflammation and pyroptosis in pulmonary epithelial cells via mediation of TNFAIP3/NF-κB axis

BACKGROUND: The progression of sepsis seriously threatens people's life. In addition, acute lung injury can contribute to the injury of epithelial cells. Meanwhile, oleanic acid can inhibit the inflammatory responses in ALI, while the mechanism underlying the function of oleanic acid remains unclear. METHODS: For investigating the impact of oleanic acid in ALI, pulmonary epithelial cells were treated with LPS. Then, CCK8 assay was employeed to detect the cell viability. RT-qPCR and western blot were applied for testing the mRNA and protein levels, respectively. Furthermore, ELISA was used to test the inflammatory factors in pulmonary epithelial cells. RESULTS: upregulation of NLRP3, ASC, cleaved caspase-1 and cleaved GSDMD, which was reversed by oleanic acid. In addition, oleanic acid notably reversed LPS-activated NF-κB signaling in cells. LPS obviously inhibited the level of TNFAIP3 in pulmonary epithelial cells, which was significantly reversed by oleanic acid. Knockdown of TNFAIP3 aggravated LPS-caused inflammation in pulmonary epithelial cells through activation of NF-κB signaling. CONCLUSION: mediation of TNFAIP3/NF-κB axis, which may serve as a new agent against ALI.