Artemisinin mimics calorie restriction to trigger mitochondrial biogenesis and compromise telomere shortening in mice

PeerJ. 2015 Mar 5;3:e822. doi: 10.7717/peerj.822. eCollection 2015.

Abstract

Calorie restriction is known to extend lifespan among organisms by a debating mechanism underlying nitric oxide-driven mitochondrial biogenesis. We report here that nitric oxide generators including artemisinin, sodium nitroprusside, and L-arginine mimics calorie restriction and resembles hydrogen peroxide to initiate the nitric oxide signaling cascades and elicit the global antioxidative responses in mice. The large quantities of antioxidant enzymes are correlated with the low levels of reactive oxygen species, which allow the down-regulation of tumor suppressors and accessory DNA repair partners, eventually leading to the compromise of telomere shortening. Accompanying with the up-regulation of signal transducers and respiratory chain signatures, mitochondrial biogenesis occurs with the elevation of adenosine triphosphate levels upon exposure of mouse skeletal muscles to the mimetics of calorie restriction. In conclusion, calorie restriction-triggered nitric oxide provides antioxidative protection and alleviates telomere attrition via mitochondrial biogenesis, thereby maintaining chromosomal stability and integrity, which are the hallmarks of longevity.

Keywords: Artemisinin; BRCA1; Calorie restriction; Hydrogen peroxide; Nitric oxide; Telomere.

Grant support

Financial support was provided by the National Science Foundation of China (NSFC). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.