2. Academic Validation
  3. Araloside C protects H9c2 cardiomyoblasts against oxidative stress via the modulation of mitochondrial function

Araloside C protects H9c2 cardiomyoblasts against oxidative stress via the modulation of mitochondrial function

  • Biomed Pharmacother. 2019 Sep:117:109143. doi: 10.1016/j.biopha.2019.109143.
Min Wang 1,  Ruiying Wang 1,  Xueheng Xie 2,  Guibo Sun 3,  Xiaobo Sun 4
Affiliations

Affiliations

  • 1 Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100193, PR China.
  • 2 Harbin University of Commerce, Harbin, 150076, Heilongjiang, PR China.
  • 3 Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100193, PR China. Electronic address: [email protected].
  • 4 Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100193, PR China. Electronic address: [email protected].
PMID: 31387189 DOI: 10.1016/j.biopha.2019.109143
Abstract

Araloside C (AsC) has potential cardioprotective properties. However, the underlying mechanism of AsC-mediated cardioprotection, especially the role of mitochondrial function, remains largely unknown. Here, we used H9c2 cardiomyocytes to study the cardioprotective mechanisms of AsC through H2O2-induced oxidative stress. Cell viability, Lactate Dehydrogenase release, mitochondrial functions and bioenergetics were evaluated. Western blot analysis was used to measure the protein expression levels of Apoptosis and the phosphorylation of AMP-activated protein kinase (AMPK). Results revealed that AsC increased cell viability, improved mitochondrial membrane potential disruption, decreased mitochondrial Reactive Oxygen Species level, elevated cellular ATP levels and alleviated impaired mitochondrial respiration in H2O2-induced H9c2 cardiomyoblasts injury. Furthermore, AsC modulated apoptosis-associated protein expression and AMPK pathway in H9c2 cells under oxidative stress. In conclusion, AsC potentially protects H9c2 cardiomyoblasts against oxidative stress by regulating mitochondrial function and AMPK activation. AsC may be an effective therapeutic agent for the prevention of oxidative stress in cardiac injury.

Keywords

AMPK; Araloside C; Cardioprotection; Mitochondrial function.

Figures
Products