Research Paper Volume 10, Issue 9 pp 2338—2355
Antioxidant modifications induced by the new metformin derivative HL156A regulate metabolic reprogramming in SAMP1/kl (-/-) mice
Figure 3. Effects of HL156A on ROS production, mitochondrial membrane potential, and aging in SAMP1/kl-deficient MEFs. (A, B) ROS production in SAMP1/kl+/+ and SAMP1/kl-/- MEFs. ROS levels were measured in SAMP1/kl+/+ and SAMP1/kl-/- MEFs treated with/without HL156A (20 or 30 μM). Cells were viewed using fluorescence microscopy. The graph was derived from 3 independent experiments. (C) Effect of HL156A on mitochondrial membrane potential activity in SAMP1/kl-/- MEFs. Cells were incubated with 20 μM HL156A for 24 h, and the level of the fluorogenic probe JC-1 was then determined to analyze mitochondrial membrane potential. (D) Effect of HL156A on aging in SAMP1/kl-/- MEFs. SAMP1/kl-/- MEFs were exposed to 20 μM HL156A for 24 h. Cell senescence was analyzed with senescence-associated β-galactosidase (SA-β-gal) staining.