氧化应激
MAPK/ERK通路
p38丝裂原活化蛋白激酶
生物
炎症
细胞生物学
线粒体
磷酸化
活力测定
活性氧
激酶
药理学
细胞凋亡
免疫学
生物化学
作者
Wei Sun,Ming Liu,Yanqiu Li,Xiaochun Hu,Guangsheng Chen,Fa‐Li Zhang
出处
期刊:Tissue & Cell
[Elsevier]
日期:2023-07-19
卷期号:84: 102170-102170
被引量:3
标识
DOI:10.1016/j.tice.2023.102170
摘要
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.
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