Abstract
Methylmercury (MeHg) exposure can cause nerve damage and mitochondrial dysfunction. Mitochondrial dysfunction is mainly mediated by mitochondrial biogenesis and mitochondrial dynamics disorders. Quercetin (QE) plays an important role in activating silencing information regulator 2 related enzyme 1 (SIRT1), and SIRT1 activates peroxisome-proliferator-activated receptor-γ co-activator 1α (PGC-1α), which can regulate mitochondrial biogenesis and mitochondrial dynamics. The main purpose of this study was to explore the alleviating effects of QE on MeHg-induced nerve damage and mitochondrial dysfunction. The results showed that QE could reduce the excessive production of reactive oxygen species (ROS) and the loss of membrane potential induced by MeHg. Meanwhile, QE activated SIRT1 activity and SIRT1/PGC-1α signaling pathway, improved mitochondrial biogenesis and fusion and reduced mitochondrial fission. In summary, we hypothesized that QE prevents MeHg-induced mitochondrial dysfunction by activating SIRT1/PGC-1α signaling pathway.
Acknowledgements
We thank the Experimental Technology Center of the School of Public Health of China Medical University for its technical support.
Author contributions
Haihui Liu: conceptualized and designed the work; performed laboratory experiments; analyzed and interpreted the data; wrote the draft and final versions of the manuscript. Liujiangshan Jiang: conceptualized and designed the work; performed laboratory experiments; wrote the final versions of the manuscript. Si Xu: performed laboratory experiments; analyzed and interpreted the data. Chen Wang: conceptualized and designed the work; performed laboratory experiments; Jingyi Sun: conceptualized and designed the work; wrote the final approval of the version to be published. All authors read and approved the final version of the manuscript.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The interpretation of results obtained from the experiments is included in this publication.