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Polygonatum polysaccharide (PP) has good myocardial protection. This study aims to find whether PP can relieve inflammation and play a protective role in diabetic cardiomyopathy (DCM). Intraperitoneal injection of streptozotocin was used to induce DCM in rats, which were then separated into four groups: model group, PP-200 group (200 mg/kg PP), PP-400 group (400 mg/kg PP), and Met group (120 mg/kg metformin). Both control (NC) and model groups of rats were administered normal saline. According to the kit instructions mentioned on the kit, the levels of blood glucose, glycosylated hemoglobin, insulin (INS), and myocardial enzymes (creatinine kinase, B-type natriuretic peptide, and cardiac troponin I) were measured after 8 weeks. Cardiac function was detected by echocardiography. Hematoxylin and eosin (HE) and Masson staining were used to observe pathological changes. Myocardial RNA and protein levels of NLR family pyrin domain containing 3 (NLRP3), caspase-1, and Gasdermin D (GSDMD) were quantified through reverse transcription-polymerase chain reaction and Western blotting analysis. The in vivo findings showed that PP could reduce blood glucose, glycosylated hemoglobin, and INS levels, enhance heart functioning, restore histological alterations and myocardial enzymes, and relieve myocardial fibrosis. Furthermore, PP suppressed the expressions of NLRP3, caspase-1, and GSDMD. PP could reduce inflammation in DCM rats by suppressing NLRP3 inflammasome.

Sheng Mai Yin (SMY) has therapeutic effects on myocardial infarction (MI), heart failure (HF), diabetic cardiomyopathy (DCM), and myocarditis. To study whether SMY can relieve pyroptosis and play a protective role in diabetic cardiomyopathy, a molecular docking technique was used to predict the possible mechanism of SMY against DCM. Then, a DCM rat model was induced by intraperitoneal injection of streptozotocin (STZ), divided into 5 groups: the DM group (model), SMY-L group (2.7 mL/kg SMY), SMY-M group (5.4 mL/kg SMY), SMY-H group (10.8 mL/kg SMY), and Met group (120 mg/kg metformin). Rats in the CTL group (control) and DM group were given normal saline. After 8 weeks, the levels of blood glucose, lipids, and myocardial enzymes were detected according to the kit instructions. Cardiac function was detected by echocardiography. HE and Masson were used to observing the pathological changes, collagen deposition, and collagen volume fraction (CVF). The apoptosis rate of cardiomyocytes was determined by Tunel. The IL-1β level was determined by ELISA and RT-PCR. The expressions of NLRP3, caspase-1, and GSDMD were measured using RT-PCR and Western blotting. The docking results suggested that SMY may act on NLRP3 and its downstream signal pathway. The in vivo results showed that SMY could reduce blood glucose and lipid levels, improve heart function, improve histopathological changes and myocardial enzymes, and alleviate cardiomyocyte apoptosis and myocardial fibrosis. SMY inhibited the mRNA and protein expressions of NLRP3, ASC, Caspase-1, and GSDMD and IL-1β production. SMY can reduce DCM by regulating the NLRP3/caspase-1 signaling pathway, providing a new research direction for the treatment of DCM.

Context Punicalagin has myocardial protection; the mechanism of punicalagin on ventricular remodeling (VR) after acute myocardial infarction (AMI) remains unclear. Objective These studies explore the role and mechanism of punicalagin in preventing and treating VR after AMI. Materials and methods Molecular docking was used to predict the targets of punicalagin. After 2 weeks of AMI model, the SD rats were randomly divided into model, and punicalagin (200, 400 mg/kg, gavage) groups for 4 weeks. Thoracotomy with perforation but no ligature was performed on rats in control group. The protein expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis speck-like protein (ASC), caspase-1, gasdermin D (GSDMD), and GSDMD-N, the mRNA expression of NLRP3, caspase-1, GSDMD, interleukin-1β (IL-1β) and IL-18 were evaluated. Results Punicalagin had binding activities with NLRP3 (Vina score, −5.8), caspase-1 (Vina score, −6.7), and GSDMD (Vina score, −6.7). Punicalagin could improve cardiac function, alleviate cardiac pathological changes, minimize the excessive accumulation of collagen in the left ventricular myocardium ( p < 0.01), and inhibit cardiomyocyte apoptosis ( p < 0.01). Furthermore, punicalagin could inhibit the overexpression of NLRP3, caspase-1, and GSDMD via immunohistochemistry ( p < 0.01). Punicalagin inhibited the protein levels of NLRP3, caspase-1, ASC, GSDMD, and GSDMD-N ( p < 0.05, p < 0.01). Punicalagin reduced the mRNA expression of NLRP3, caspase-1, GSDMD, IL-1β and IL-18 ( p < 0.05, p < 0.01). Conclusions Punicalagin may provide a useful treatment for the future myocardial protection.

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