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Front Pharmacol. 2018 Feb 20;9:107. doi: 10.3389/fphar.2018.00107. eCollection 2018.

Autophagy Flux Contributes to Regulation of Components of Eclipta prostrata L. on Cigarette Smoking-Induced Injury of Bronchial Epithelial Cells.

Ding S1, Hou X2,3, Wang G2,3, Qiu H2, Liu Y2,3, Zhou Y2, Du M2,3, Tan X2, Song J2, Wei Y2, Shu L2, Li Z4, Feng L2,5, Jia X2,5,6.

Author information

1
School of Pharmaceutical Engineering and Life Science, Changzhou University, Changzhou, China.
2
Key Laboratory of New Drug Delivery System of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Nanjing, China.
3
College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei, China.
4
China Minority Traditional Medical Center, Minzu University of China, Beijing, China.
5
College of Traditional Chinese Medicine, China Pharmaceutical University, Nanjing, China.
6
Affliated Hospital of Long Hua, Shanghai University of Chinese Medicine, Shanghai, China.

Abstract

Excessive autophagy plays a crucial role in cigarette smoking extract (CSE)-induced inflammation response and oxidative damage of respiratory epithelial cells. The components from Eclipta prostrata L. (CCE) have been shown to be beneficial for CSE-induced epithelial cells injury. However, whether its protection on CSE-stress injury is related to its regulation on autophagy remains still unclear. In this study, CCE, containing mainly wedelolactone of 45.88% and demethylwedelolactone of 23.74%, could improve significantly 10%CSE-induced cell viability of normal human bronchial epithelial (NHBE) cells using CCK-8 kit. We revealed that CCE could remarkably increase autophagic factors Beclin-1, Atg5, ATF4 proteins expression levels and the transformation of LC3-I to LC3-II. Additionally, CCE up-regulated significantly p-p16 and p-p21 phosphorylation levels whereas down-regulated p-p53 in NHBE cells. The changes of typical autolysosom and representative autophagosome in the presence of CCE or/and autophagy inhibitor chloroquine (CQ) were also observed by transmission electron microscopy. These data demonstrated that CCE reduced CSE-induced autophagy flux activation in NHBE cells. The blockade of CCE on autophagy flux contributes to its protection against CSE-induced NHBE cells damage, and CCE is promising to be combination therapeutic molecules to excessive autophagic damage in respiratory diseases.

KEYWORDS:

Eclipta prostrata L.; autophagy; bronchial epithelial cells; cigarette smoking; stress injury

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