Xanthorrhizol inhibits mitochondrial damage, oxidative stress and inflammation in LPS-induced MLE-12 cells by regulating MAPK pathway

Abstract

LPS-induced injury in lung epithelial cells is a crucial part of the process of acute lung injury (ALI). The aim of this study is to explore whether Xanthorrhizol, a medicine that has antioxidant and anti-inflammatory activity, could mitigate the injury of lung epithelial cells caused by LPS. Mouse lung epithelial cell line (MLE-12 cells) were treated with LPS in the absence and presence of Xanthorrhizol. As a results, we observed that LPS could induce MLE-12 cells death, mitochondrial dysfunction, oxidative stress and inflammation, and activate MAPK signaling pathways. However, Xanthorrhizol mitigated the injury in MEL-12 caused by LPS by promoting cell viability and MDA, GSH production as well as inhibiting LDH release, mitochondria damage, IL-1β, IL-6 and TNF-α production and the phosphorylation levels of ERK, P38 and JNK. Our results indicated that Xanthorrhizol could protect lung epithelial cells from LPS-induced injury, more likely by inhibiting the phosphorylation of MAPK pathway related proteins.

Keywords: Acute lung injury; Inflammation; Mitochondrial injury; Oxidative stress; Xanthorrhizol.