Quercetin Protects Rat L6 Myocytes from Antimycin A-Induced Mitochondrial DysfunctionVijay M Kale*
College of Pharmacy, Roseman University of Health Sciences, South Jordan, Utah
- *Corresponding Author:
- Vijay M. Kale
Assistant Professor of Pharmaceutical Sciences
College of Pharmacy
Roseman University of Health Sciences
South Jordan, Utah
E-mail: [email protected]
Received date: December 28, 2015; Accepted date: January 25, 2016; Published date: January 28, 2016
Citation: Kale VM (2016) Quercetin Protects Rat L6 Myocytes from Antimycin A-Induced Mitochondrial Dysfunction. Clin Exp Pharmacol 6:202. doi: 10.4172/2161-1459.1000202
Copyright: © 2016 Kale VM. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objective: Mitochondrial dysfunction is often associated with various disorders such as diabetes, Alzheimer’s etc. Reactive oxygen species (ROS), aging, and reduction of mitochondrial biogenesis contribute to mitochondrial dysfunction. Antimycin-A (AMA) damages the mitochondria through inhibition of mitochondrial electron transport. The present study sought to investigate effects of quercetin on rat L6 cells and whether quercetin protects mitochondria against oxidative damage caused by AMA. Methods: Rat L6 myocytes were used for the study. Effects of quercetin on Antimycin-A induced mitochondrial dysfunction was studied using cytotoxicity, ATP levels, mitochondrial superoxide production and NDUFB8 mRNA expression. Results: In this study, exposure of L6 myocytes to AMA induced an increase cell death, decreased ATP content, followed by a decrease in mitochondrial superoxide, and decreased expression of NDUFB8. We found that quercetin protected myocytes from antimycin-A (AMA) induced L6 cell death as evidenced from increased lactate dehydrogenase (LDH) leakage into extracellular medium, protected ATP production, prevented increase in oxidative stress and restored levels of NDUFB8 mRNA expression implying improved mitochondrial function. Conclusion: These results suggest that the quercetin showed protective effect against AMA-induced mitochondrial dysfunction by increasing ATP production, decreasing oxidative stress, and restoring mitochondrial function.