Mogroside IIE,an in vivo metabolite of sweet agent,alleviates acute lung injury via Pla2g2a-EGFR inhibition

脂多糖 下调和上调 药理学 化学 PI3K/AKT/mTOR通路 表皮生长因子受体 代谢物 癌症研究 医学 受体 信号转导 免疫学 生物化学 基因
作者
Weichao Lü,Guoqing Ren,Kuniyoshi Shimizu,Renshi Li,Chaofeng Zhang
标识
DOI:10.26599/fshw.2022.9250025
摘要

In the face of increasingly serious environmental pollution, the health of human lung tissues is also facing serious threats. Mogroside ⅡE (M2E) is the main metabolite of sweetening agents mogrosides from the anti-tussive Chinese herbal Siraitia Grosvenori. The study elucidated the anti-inflammatory action and molecular mechanism of M2E against acute lung injury (ALI). A lipopolysaccharide (LPS)-induced ALI model was established in mice and MH-S cells were employed to explore the protective mechanism of M2E through the western blotting, co-immunoprecipitation, and quantitative real time-PCR analysis. The results indicated that M2E alleviated LPS-induced lung injury through restraining the activation of Secreted phospholipase A2 type IIA (Pla2g2a) -Epidermal Growth Factor Receptor (EGFR). The interaction of Pla2g2a and EGFR was identified by co-immunoprecipitation. In addition, M2E protected ALI induced with LPS against inflammatory and damage which were significantly dependent upon the downregulation of AKT and mTOR via the inhibition of Pla2g2a-EGFR. Pla2g2a may represent a potential target for M2E in the improvement of LPS-induced lung injury, which may represent a promising strategy to treat ALI.
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