Polysaccharides Attenuate Cardiac Injury by Inhibiting CaMKII-Mediated P38/NF-[Formula: see text]B/NLRP3 Signaling Pathway to Reduce Sepsis-Induced Apoptosis and Inflammation.

Sepsis is a life-threatening condition characterized by systemic inflammatory response syndrome, and often results in cardiac damage and poor prognosis. This study aimed to explore the protective effects of polysaccharides (PCP) on sepsis-induced cardiac injury and elucidate the underlying molecular mechanisms. An sepsis model was established, and an myocardial cell model was induced using lipopolysaccharide (LPS) to mimic a sepsis environment. Histopathological analysis revealed morphological changes in the myocardial tissue, while apoptosis and oxidative stress in the myocardial cells were assessed using immunofluorescence staining. The Western blot assay was employed to measure the expression levels of CaMKII, NF-[Formula: see text]B, and NLRP3, and myocardial cell apoptosis was quantified by flow cytometry. Inflammatory cytokine levels were determined via ELISA. The results indicated that PCP treatment significantly alleviated myocardial injury, reduced myocardial apoptosis, and lowered the levels of inflammatory markers when compared to the sepsis group. Mechanistic studies revealed that PCP inhibited the P38/NF-[Formula: see text]B/NLRP3 signaling pathway activation induced by CaMKII to thereby mitigate apoptosis and the inflammatory response in sepsis-induced cardiomyocytes. In conclusion, PCP exerts a protective effect against sepsis-induced cardiac injury by inhibiting the CaMKII-mediated P38/NF-[Formula: see text]B/NLRP3 signaling pathway. This study provides a novel theoretical framework and identifies potential therapeutic targets for the prevention and treatment of sepsis-associated cardiac injury.