Neferine Enhances Autophagy to Alleviate Cytotoxicity and Apoptosis Induced by CSE in AEC-II through AMPK/mTOR Signaling Pathway

Abstract

COPD is a clinical common chronic respiratory disease, its incidence case fatality rate is higher, there is currently no cure drugs and methods. In this study, in order to make clear its role in the development of autophagy in COPD, COPD cell model is established.To further explore whether regulating autophagy could have a protective effect to fight against CSE-induced cytotoxicity and apoptosis, we choose neferine as an autophagy inducer. Neferine activated cell autophagy in an vitro CSE-induced COPD cell model and gradually attenuated CSE-induced cell apoptosis. Furthermore, this process happens largely through the AMPK/mTOR signaling pathway. As a autophagic flux inhibitor, chloroquine abolished the prosurvival autophagy effect, and AMPK inhibitor Compound C blocked neferine-mediated autophagy and then neferine failed to protect COPD cell model from CSE-induced apoptosis. Overall,our findings suggested that neferine possibly has a potentially protective effect in cell damage mechanisms caused by CSE. It hints that neferine has the prospect of turning into a potential therapeutics to cure CSE-induced cytotoxicity and apoptosis and even COPD patients.