The present method has anti-aging properties against high-glucose. The present invention reveals the anti-aging properties of antcin M (ANM) and elucidates the molecular mechanism underlying the effects. It is found that exposure of human normal dermal fibroblasts (HNDFs) to high-glucose (HG) for 3 days, cell phase arrest and senescence are accelerated. As confirmed through experiments, co-treatment with ANM significantly attenuates HG-induced growth arrest and promotes cell proliferation. In addition, treatment with ANM eliminates HG-induced reactive oxygen species through the induction of anti-oxidant genes via transcriptional activation of NF-E2 related factor-2 (Nrf2). Treatment with ANM abolishes HG-induced stress-induced premature senescence as evidenced by reduced senescence-associated β-galactosidase activity. Also, the HG-induced decline in aging-related marker protein, senescence marker protein-30, is rescued by ANM. Furthermore, treatment with ANM increases expression of silent mating type information regulation 2 homologs 1 (SIRT-1), and prevents SIRT-1 depletion.
