Effect of Asterone on LPS-induced Inflammation and Autophagy in Airway Cells
10.3870/j.issn.1672-0741.22.04.031
- VernacularTitle:紫菀酮对LPS诱导的气道细胞炎症反应及自噬的影响
- Author:
Zhen LI
1
;
Kui AI
Author Information
1. 武汉市第三医院光谷院区儿科,武汉 430074
- Keywords:
asterone;
inflammation;
autophagy;
Beas-2B cell
- From:
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
2023;52(6):791-795,822
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of asterone on airway epithelial cell autophagy and its mechanism through LPS-induced airway epithelial cell inflammation model.Methods Beas-2B cells(human bronchial epithelial cells)were induced by LPS to construct an inflammation model.The effect of asterone on the proliferative activity of Beas-2B cells was detected by CCK-8.The levels of IL-6 and TNF-a in the cells were detected by ELISA.The expression levels of NF-κB and AP-1 in each group of cells were detected by RT-PCR.The relative expression of NF-κB、p-NF-κB、AP-1、Beclin 1、LC3-Ⅱ、LC3-Ⅰ、mTOR、p-mTOR、p-S6K1 and S6K1 was detected by Western blotting.The changes of autophagy in each group of cells were observed by acridine orange staining.Results Compared with the control group,the relative expression of AP-1 and p-NF-κB was signifi-cantly higher than that of LPS group(P＜0.05);orange and red fluorescence with many dotted red spots of acidic membrane vesicles as well as increased autophagy level were observed in cells;the relative expressions of Beclin 1 and LC3-Ⅱ were signifi-cantly increased in cells(P＜0.05),and expressions of LC3-Ⅰ,p-mTOR and p-S6K1 were significantly reduced(P＜0.05).Compared with the LPS group,the relative expressions of AP-1 and p-NF-κB in the LPS+asterone group were significantly de-creased(P＜0.05);less orange and red fluorescence was observed in cells,and the level of autophagy was decreased(P＜0.05).The relative expressions of Beclin 1 and LC3-Ⅱ were reduced(P＜0.05).The expressions of LC3-Ⅰ,p-mTOR and p-S6K1 were increased.Conclusion Asterone can inhibit the occurrence of autophagy in Beas-2B inflammatory cells,and the mechanism may be related to activation of mTOR signaling pathway.
