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 5. HL156A-mediated changes in intermediates of glutathione metabolism. (A) The levels of intermediates of glutathione metabolism were plotted on pathway maps. The relative quantities of the detected metabolites are represented as bar graphs (from left to right: SAMP1/kl+/+ (blue), SAMP1/kl-/- (red), and HL156A-treated SAMP1/kl-/- (green) kidneys). (B) Comparisons of the relative amounts of glutathione metabolites between SAMP1/kl+/+, SAMP1/kl-/-, and HL156A-treated SAMP1/kl-/- mouse kidneys. (C) In vivo effect of HL156A administration on glutathione status in SAMP1/kl-/- mice. Oxidized (GSSG)/reduced (GSH) ratios in mouse kidneys and livers obtained from SAMP1/kl+/+ or SAMP1/kl-/- mice. (D) GSSG/GSH ratios in mouse kidneys obtained from mice orally administered 0.9% saline solution (control) or 30 mg/kg HL156A every other day for 12 weeks. GSH and GSSG levels were quantified by spectrophotometry, and GSSG/GSH ratios were calculated as estimates of oxidative stress. (E) In vitro effect of HL156A on GSSG/GSH ratios in H2O2-treated MEF kl-/- cells. H2O2-treated cells were co-incubated with 20 or 40 μM HL156A for 36 h. *p<0.05. **p<0.001.