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Poria cocos Polysaccharides Attenuate Cardiac Injury by Inhibiting CaMKII-Mediated P38/NF-[Formula: see text]B/NLRP3
Manqi Yang1,2,3, Bo Cui1,2,3, Shan Hu4
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Insights
Poria cocos polysaccharides (PCP) protect against sepsis-induced heart damage by inhibiting the CaMKII-P38/NF-κB/NLRP3 pathway, reducing cell death and inflammation.
Area of Science:
- Cardiovascular Biology
- Immunology
- Pharmacology
Background:
- Sepsis frequently causes cardiac damage, leading to poor patient outcomes.
- Understanding the molecular mechanisms of sepsis-induced cardiotoxicity is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the cardioprotective effects of Poria cocos polysaccharides (PCP) against sepsis-induced cardiac injury.
- To elucidate the molecular pathways targeted by PCP in mitigating sepsis-related heart damage.
Main Methods:
- Established in vivo sepsis and in vitro lipopolysaccharide (LPS)-induced myocardial cell models.
- Assessed myocardial injury, apoptosis, and oxidative stress using histopathology, immunofluorescence, and flow cytometry.
- Analyzed key signaling pathway proteins (CaMKII, NF-κB, NLRP3) and inflammatory cytokines via Western blot and ELISA.
Main Results:
- PCP treatment significantly reduced myocardial injury, apoptosis, and inflammatory markers in sepsis models.
- PCP inhibited the CaMKII-mediated activation of the P38/NF-κB/NLRP3 signaling pathway.
- These effects collectively mitigated apoptosis and inflammation in sepsis-induced cardiomyocytes.
Conclusions:
- Poria cocos polysaccharides (PCP) demonstrate significant cardioprotective effects against sepsis.
- PCP acts by inhibiting the CaMKII-P38/NF-κB/NLRP3 signaling pathway, offering a novel therapeutic strategy.
- This study identifies potential targets for preventing and treating sepsis-associated cardiac injury.
Abstract:
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 Poria cocos polysaccharides (PCP) on sepsis-induced cardiac injury and elucidate the underlying molecular mechanisms. An in vivo sepsis model was established, and an in vitro 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.
