臨床および実験薬理学ジャーナル

概要

Quercetin Protects Rat L6 Myocytes from Antimycin A-Induced Mitochondrial Dysfunction

Vijay M Kale*

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.