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.
Highlights
Cigarette smoking has been regarded as a high risk factor in the pathogenesis of lung diseases, and plays a contributor to the molecular events in carcinogenesis of bronchial epithelial cells (Nyunoya et al, 2014)
The aim of this study is to explore the regulation of CCE on autophagy of cigarette smoking-induced stress injury of bronchial epithelial cells, and reveal the possible mechanism
It has been demonstrated that autophagy plays a critical role in maintenance of cellular homeostasis and the adaption to environmental stress such as oxidative stress, starvation, hypoxia and infection (Gansukh et al, 2016; Zeng et al, 2016; Aseer et al, 2017; Guo et al, 2017)
Summary
Cigarette smoking has been regarded as a high risk factor in the pathogenesis of lung diseases, and plays a contributor to the molecular events in carcinogenesis of bronchial epithelial cells (Nyunoya et al, 2014). Evidence showed that the stress injury caused by cigarette smoking condensate is thought to be related to the imbalance of homeostasis of normal lung epithelial cells (Yu et al, 2016). Cigarette smoking stimulates normal human bronchial epithelial (NHBE). Autophagy of CCE to NHBE cells which cause a multistep process involving morphologic and molecular modifications. The cigarette smoke-induced stress injury is involved in oxidative stress, inflammation response, autophagy activation, and so on. Continuous cigarette smoking increases the probability to absolute mortality risk of various lung diseases for individuals, leading to greater public health problems (Lewer et al, 2017)
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call