Dendropanax morbifera Extract Protects Cardiomyocytes against Hypoxia/Reoxygenation Injury by Inhibition of Reactive Oxygen Species Generation and Calcium Perturbation
10.20307/nps.2019.25.2.136
- Author:
Leejin LIM
1
;
Sujin JU
;
Heesang SONG
Author Information
1. Depatment of Biomedical Sciences, Chosun University Graduate School, Gwangju 61452 Korea. hsong@chosun.ac.kr
- Publication Type:Original Article
- Keywords:
Dendropanax morbifera;
hypoxia/reoxygenation;
cardiomyocytes
- MeSH:
Animals;
Blotting, Western;
Calcium;
Communicable Diseases;
Headache;
Heart;
Homeostasis;
Myocardial Infarction;
Myocytes, Cardiac;
Rats;
Reactive Oxygen Species;
Ryanodine Receptor Calcium Release Channel
- From:Natural Product Sciences
2019;25(2):136-142
- CountryRepublic of Korea
- Language:English
-
Abstract:
Ischemia/reperfusion-induced myocardial injury is the main cause of acute myocardial infarction. Dendropanax morbifera Léveille has been used in traditional medicines for the treatment of various diseases such as headache, infectious diseases, and general debility. However, the effect of extract from D. morbifera (EDM) on myocardial ischemic injury is still unknown. In this study, the effects of EDM on neonatal rat cardiomyocytes with hypoxia/reoxygenation (H/R) injury were investigated. The viability of cardiomyocytes with H (30 min)/R (1 h) decreased; however, treatment with EDM significantly inhibited H/R injury-induced cardiomyocyte death. Further, we observed that reactive oxygen species (ROS) generation and intracellular calcium concentration (Ca²⁺ᵢ) were significantly reduced in EDM-treated cardiomyocytes compared with that in H/R-injured positive control. In addition, western blotting results showed that EDM attenuated abnormal changes of RyR2 and SERCA2a genes in hypoxic cardiomyocytes. These results suggest that EDM ameliorates ROS generation and Ca²⁺ᵢ homeostasis to prevent dysregulation of calcium regulatory proteins in the heart, thereby exerting cardioprotective effects and reducing hypoxia-induced cardiomyocyte damage, which verifies the potential use of EDM as a new therapeutic agent for the treatment of myocardial ischemic injury.
