Fig. 2. Melatonin improved oxidative stress and mitochondrial membrane potential by lowering mitochondrial HK2 expression in chronic kidney disease mouse model-derived mesenchymal stem cells (CKD-mMSCs). (A) Immunoblotting results showing the expression of HK1 and HK2 in each experimental mMSC group: untreated CKD-mMSCs, CKD-mMSCs treated with melatonin, and melatonin-treated CKD-mMSCs pre-treated with luzindole. Expression levels of HK1 and HK2 were normalized relative to VDAC1 levels. Values represent the mean ± SEM (n=3). *p<0.05 or **p<0.01 vs. control; ##p<0.01 vs. melatonin-treated CKD-mMSCs. (B) CKD-mMSCs from each experimental group assayed using MitoSOX to assess mitochondrial oxidative stress. MitoSOX signals were quantified using flow cytometry. Values represent the mean ± SEM (n=5). **p<0.01 vs. control, ##p<0.01 vs. melatonin-treated CKD-mMSCs. (C) CKD-mMSCs from each experimental group assayed using TMRE to assess mitochondrial membrane potential. TMRE signals were quantified using flow cytometry. Values represent the mean ± SEM (n=5-6). **p<0.01 vs. control, ##p<0.01 vs. melatonin-treated CKD-mMSCs.
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