학술논문

Coptisine protects cardiomyocyte against hypoxia/reoxygenation-induced damage via inhibition of autophagy.
Document Type
Article
Source
Biochemical & Biophysical Research Communications. Aug2017, Vol. 490 Issue 2, p231-238. 8p.
Subject
*ISOQUINOLINE
*AUTOPHAGY
*HEART cells
*HYPOXEMIA
*APOPTOSIS
Language
ISSN
0006-291X
Abstract
Coptisine is a natural occurring isoquinoline alkaloid isolated from the traditional Chinese medicinal herb Rhizoma coptidis . Coptisine has been reported to have protective effects on reperfusion injury in cardiomyocytes, however, the underlying mechanism remains uncertain. Here, we used a hypoxia/reoxygenation (H/R)-treated H9c2 cell model to study the protective effects of coptisine on cardiomyocyte. The results showed that NaS 2 O 4 induced hypoxia/reoxygenation model increased apoptosis and up-regulated autophagy marker LC3-II and cleaved Caspase-3, Beclin1 and Sirt1 levels. Coptisine treatment increased cell survival, inhibited apoptosis, and reduced the protein level of LC3-II, cleaved Caspase-3, Beclin1 and Sirt1. Further, we showed that coptisine combined with chloroquine (CQ), the inhibitor of autolysosome, reduced LC3-II, suggesting that coptisine may inhibit autophagosome formation than induction of autolysosome in the autophagy events. Our results indicate that coptisine may protect cardiomyocyte damage by H/R through suppressing autophagy. Overall, our study provides a new mechanism for the treatment of coptisine on H/R-induced cardiomyocyte damage and death. [ABSTRACT FROM AUTHOR]