Purpose: Myocardial ischemia/reperfusion injury (MIRI) leads to myocardial tissue necrosis, which will increase the size of myocardial infarction. The study examined the protective effect and mechanism of the Guanxin Danshen formula (GXDSF) on MIRI in rats. Methods: MIRI model was performed in rats; rat H9C2 cardiomyocytes were hypoxia-reoxygenated to establish a cell injury model. Results: The GXDSF significantly reduced myocardial ischemia area, reduced myocardial structural injury, decreased the levels of interleukin (IL-1β, IL-6) in serum, decreased the activity of myocardial enzymes, increased the activity of superoxide dismutase (SOD), and reduced glutathione in rats with MIRI. The GXDSF can reduce the expression of nucleotide- binding oligomerization domain, leucine-rich repeat and pyrin domain containing nod-like receptor family protein 3 (NLRP3), IL-1β, caspase-1, and gasdermin D (GSDMD) in myocardial tissue cells. Salvianolic acid B and notoginsenoside R1 protected H9C2 cardiomyocytes from hypoxia and reoxygenation injury and reduced the levels of tumor necrosis factor α (TNF-α) and IL-6 in the cell supernatant, decreasing the NLRP3, IL-18, IL-1β, caspase-1, and GSDMD expression in H9C2 cardiomyocytes. GXDSF can reduce the myocardial infarction area and alleviate the damage to myocardial structure in rats with MIRI, which may be related to the regulation of the NLRP3. Conclusions: GXDSF reduces MIRI in rat myocardial infarction injury, improves structural damage in myocardial ischemia injury, and reduces myocardial tissue inflammation and oxidative stress by lowering inflammatory factors and controlling focal cell death signaling pathways.
Shenkang injection (SKI) has been widely used in the clinical treatment of chronic kidney diseases in China because of its efficacy and safety. However, the underlying mechanism of SKI in diabetic nephropathy (DN) remains unclear. The present study aimed to investigate the renoprotective effects and possible mechanisms of SKI in diabetic db/db mice. We showed that SKI ameliorated hyperglycemia and abnormal renal biochemical parameters in db/db mice. Crotonylome and subsequent bioinformatics analyses indicated that the molecular functions of the significantly different crotonylated proteins regulated by SKI were closely related to oxidoreductase activity and oxidative phosphorylation might be one of the main pathways through which SKI functions in DN. Subsequent PRM validation of the selected crotonylated proteins confirmed these findings. In addition, we determined that SKI could regulate the expression of specific proteins in oxidative phosphorylation complexes and enhance antioxidant capacity. Taken together, our data suggest that SKI exerted the protective effect against DN potentially through reversing the abnormal crotonylation expression of oxidoreductase-related proteins.
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