Key result
Ginsenoside Rh7 improves cardiac function in diabetic cardiomyopathy mice by promoting M2 macrophage polarization.
Why the study?
The study was conducted to investigate the intervention effect of ginsenoside Rh7 on myocardial dysfunction in diabetic cardiomyopathy.
Does ginsenoside Rh7 ameliorate myocardial injury and improve cardiac function in a mouse model of diabetic cardiomyopathy?
Does ginsenoside Rh7 ameliorate myocardial injury and improve cardiac function in a mouse model of diabetic cardiomyopathy?
p-value: p=<0.05
Ginsenoside Rh7 exerts cardioprotective effects in diabetic cardiomyopathy by promoting M2 macrophage polarization through the SIRT1/FOXO1/β-catenin signaling pathway.
Hypothesis-generating for ginsenoside Rh7 in diabetic cardiomyopathy; leaves open clinical translation pending human studies.
Aim: To investigate the intervention effect of ginsenoside Rh7 on myocardial dysfunction in diabetic cardiomyopathy. Methods: A diabetic cardiomyopathy (DCM) mouse model was established using a high-fat diet combined with streptozotocin (STZ), and treated with ginsenoside Rh7. Echocardiography was used to detect changes in cardiac function in mice. Mouse body weight, heart weight, and cardiac index were measured. H&E staining was used to detect pathological changes in the heart. Tissue chemistry and fluorescence staining were used to detect the expression of CD206 and SIRT1 in the heart. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of M1/M2 cell markers. Results: Rh7 can improve cardiac dysfunction in DCM mice by inhibiting the expression of SIRT1, thereby promoting the activation of the FOXO1/β-catenin complex and M2 polarization of macrophages.In vitro iBMDM experiments showed that Rh7 can promote CD206 expression and M2 polarization of macrophages. Small molecule-protein docking and pull-down experiments confirmed the binding relationship between Rh7 and SIRT1. Conclusion: Rh7 can ameliorate myocardial injury in DCM mice by inhibiting SIRT1 and activating FOXO1/β-catenin, thereby promoting M2 polarization of macrophages.
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Han et al. (2026) studied Diabetic cardiomyopathy (n=88). Ginsenoside Rh7 vs. Untreated diabetic cardiomyopathy model mice was evaluated on Cardiac function (LVEF, LVFS) and myocardial injury (p=<0.05). Ginsenoside Rh7 ameliorated myocardial injury and improved cardiac function in diabetic cardiomyopathy mice by inhibiting SIRT1 to promote M2 macrophage polarization.
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