Fig. 12

Metformin can potentially regulate the immune-metabolic microenvironment in SCM by targeting BCS1L. A mRNA expression of potential targets in the control, SCM, and SCM–metformin groups. B–D Proteins were isolated from cardiomyocytes in the control, SCM, and SCM–metformin groups, and the levels of BCS1L and FBXO7 were determined by western blotting. E–K Analysis of HL-1 mitochondrial metabolism with Seahorse XFe96 Analyzer. OCR was monitored continuously at baseline and after adding oligomycin (2 mM), FCCP (1 mM), and R/A (0.5 mM) to compare basal respiration, maximal respiration, nonmitochondrial oxygen consumption, spare respiratory capacity, proton leak, and ATP production levels among the control, SCM, SCM–metformin, and SCM–metformin–siBCS1L groups. G–I Comparison of levels of inflammation factors among different groups (N = 6 mice or eight independent cell samples per group). *p < 0.05, **p < 0.01, ***p < 0.001