Objective: This study aimed to investigate the therapeutic effects and underlying mechanisms of Sankudiwan (SKDW) on myocardial ischemia-reperfusion injury (MIRI) in a rat model.
Materials and methods: Rats were subjected to MIRI and treated with varying doses of SKDW. The myocardial infarct size, cardiac function, histological changes, apoptosis, and inflammation were assessed using TTC staining, echocardiography, Hematoxylin and Eosin (HE) staining, TUNEL staining, and ELISA assays. We further explored SKDW's influence on cardiomyocyte mitochondria and inflammatory factor expression. Moreover, oxidative stress-related parameters and differentially expressed genes were analyzed using bioinformatics approaches.
Results: SKDW significantly reduced myocardial infarct size and improved cardiac function, demonstrating a dose-dependent therapeutic potential. It ameliorated myocardial tissue damage at the histological level, inhibited cardiomyocyte apoptosis, and mitigated inflammatory response. SKDW also enhanced mitochondrial energy metabolism and suppressed the levels of oxidative stress markers. Bioinformatics analysis identified key differentially expressed genes (DEGs), including cbln1, Tgm1, Trh, and Ccl27, possibly mediating the therapeutic effects of SKDW.
Conclusions: SKDW exerts its therapeutic effects on MIRI through the modulation of several genes and pathways related to inflammation, apoptosis, mitochondrial function, and oxidative stress. Our findings provide a scientific basis for the clinical application of SKDW in the treatment of MIRI.