Pinus massoniana pollen polysaccharides alleviate LPS-induced myocardial injury through p110β-mediated inhibition of the PI3K/AKT/NFκB pathway.

The inflammatory response is the core of the pathogenesis of lipopolysaccharide (LPS)-induced sepsis myocardial injury (SMI). Pinus massoniana pollen polysaccharide (PPPS) is a natural polymer with known biological activities, including anti-inflammatory, antioxidant, and antiviral properties. In this study, we aimed to investigate the impact of PPPS on SMI, myocardial enzyme levels, pathological changes, oxidative stress, cell apoptosis, and related signaling pathways in LPS-induced SMI models were observed by hematoxylin-eosin (HE) staining, immunohistochemical (IHC) staining, qPCR, Western blot analysis, with a particular focus on anti-inflammatory effects of PPPS. Animal experiments have shown that PPPS mitigates myocardial tissue injury and suppresses the inflammatory response. In the cellular experiments, PPPS protected H9c2 cells from LPS/adenosine triphosphate (ATP)-induced injury and inflammation. Transcriptome analysis and cardiomyocyte validation revealed that PPPS inhibited activation of the PI3K/PTEN/AKT signaling pathway. Additionally, intervention with the PI3K/PTEN/AKT signaling pathway activator counteracted the anti-inflammatory effects of PPPS. Further investigations indicated that PPPS exerts its anti-inflammatory effects in SMI by enhancing the expression of p110β protein and facilitating its interaction with PTEN, thereby inhibiting activation of the PI3K/AKT/NFκB signaling pathway. These results suggest that PPPS is a promising therapeutic agent for the treatment of SMI.