Apigenin ameliorates D-galactose-induced lifespan shortening effects via antioxidative activity and inhibition of mitochondrial-dependent apoptosis in Drosophila melanogaster

Abstract

Apigenin, a dietary flavonoid, was used to alleviate D-galactose-induced aging in Drosophila melanogaster. Flies were treated with Apigenin and D-galactose for lifespan and survival studies respectively. Similarly, flies were fed with Apigenin and D-galactose for seven days. Thereafter, flies were exposed to Apigenin and/or D-galactose for 7 days to evaluate biochemical markers. The results revealed that D-galactose-fed flies exhibited decreased locomotor activity, acetylcholinesterase (AChE) activity, Total thiol content, glutathione (GSH) level and altered activities of antioxidant enzymes. However, Apigenin prolonged the lifespan of flies and restored D-galactose-induced inhibition of catalase, glutathione S-transferase and AChE activities. Additionally, Apigenin ameliorated D-galactose-induced accumulation of hydrogen peroxide and nitrate and nitrite levels in flies. Moreover, Apigenin inhibited D-galactose-induced mitochondrial Permeability Transition (mPT) pore opening, consistent with reduction in caspases 9 (DRONC) and 3 (DrICE) activities in flies. Delay of D-galactose-induced aging by apigenin is partly due to its antioxidant property and inhibitory effect on mitochondrial-mediated apoptosis.

Keywords

• Apigenin
• Oxidative stress
• Apoptosis
• Mitochondria
• Aging
• Drosophila melanogaster