What is the clinical evidence from this study?

Study design: Other. Population: Male C57BL/6 mice aged 8-10 weeks with cecal ligation and puncture induced septic myocardial injury (n=82). Intervention: Astragalus polysaccharide nanoparticles (APS-CS/TPP) vs. Saline gavage in sham and CLP control groups. Primary outcome: Survival rate at 72 hours after CLP, cardiac function measured by LVEF, LVFS, SV, CO at 8 hours post-CLP, myocardial injury assessed by histopathology and serum markers (cTnI, CK-MB, LDH) at 48 hours (Absolute improvement in survival by 23.34% (from 33.33% to 56.67%), p=<0.05).

What question did this study set out to answer?

This research investigates how astragalus polysaccharide nanoparticles protect against myocardial injury caused by sepsis.

February 26, 2026Open Access

Astragalus Polysaccharide Nanoparticles Alleviate Sepsis-Induced Myocardial Injury by Targeting the HSP90AA1/NLRP3 Signaling Pathway

Q: What are the key findings of this study?

Astragalus polysaccharide nanoparticles (APS-CS/TPP) improved 72-hour survival by 23.3% and significantly restored cardiac function and reduced myocardial injury markers in septic mice compared to control.

Q: What question did this study set out to answer?

This research investigates how astragalus polysaccharide nanoparticles protect against myocardial injury caused by sepsis.

Resultado clave

Astragalus polysaccharide nanoparticles (APS-CS/TPP) improved 72-hour survival by 23.3% and significantly restored cardiac function and reduced myocardial injury markers in septic mice compared to control.

Puntos clave

This research investigates how astragalus polysaccharide nanoparticles protect against myocardial injury caused by sepsis.
Network pharmacology and molecular docking predicted key signaling pathways.
Astragalus polysaccharide nanoparticles were prepared and characterized.
A septic myocardial injury model was created in mice using cecal ligation and puncture (CLP).
Therapeutic effects were evaluated using echocardiography, ELISA, histology, and Western blot analysis.
In vitro H9c2 cardiac cells were treated with LPS and APS-CS/TPP to assess inflammatory markers.
Astragalus polysaccharide nanoparticles showed high binding affinity to HSP90AA1.
These nanoparticles improved survival rates and reduced myocardial damage in septic mice.
They lowered levels of inflammation markers IL-1β, IL-6, and TNF-α in vitro.
Downregulation of HSP90AA1, NLRP3, and caspase-1 was observed with nanoparticle treatment.
Effects were diminished when the HSP90AA1 inhibitor TAS-116 was used.

PICO estructurado

Does Astragalus polysaccharide nanoparticles (APS-CS/TPP) improve survival and attenuate myocardial damage in sepsis-induced myocardial injury models?

Población

C57BL/6 male mice (8-10 weeks old, n=82) with cecal ligation and puncture (CLP)-induced septic myocardial injury, and H9c2 cardiomyocyte cell line stimulated with LPS.

Intervención

Astragalus polysaccharide nanoparticles (APS-CS/TPP) 200 mg/kg by gavage daily for 3 days prior to CLP and every 6 hours for 48 hours post-CLP in mice; 50 μg/mL in H9c2 cells.

Comparador

Sham surgery with saline (mice) or PBS (cells); Model control receiving CLP + saline (mice) or LPS + PBS (cells).

Resultado

Survival rate, cardiac function (LVEF, LVFS, SV, CO), myocardial injury markers (cTnT, LDH, CK-MB), and inflammatory markers (IL-1β, IL-6, TNF-α).surrogate

Astragalus polysaccharide nanoparticles alleviate sepsis-induced myocardial injury and improve survival in mice by targeting the HSP90AA1/NLRP3 signaling pathway.

Resultado numérico

Estimación del efecto: Absolute improvement in survival by 23.34% (from 33.33% to 56.67%)

Tasa de eventos absoluta: 56.67% vs 33.33%

valor p: p=<0.05

Limitaciones

Study conducted only in young male mice which limits generalizability.
No blinding reported which may introduce bias.
Focus on acute-phase injury with limited insight into long-term cardiac function.
Preclinical animal model findings require validation in human clinical trials.

Resumen

Purpose: This study aimed to investigate the mechanisms by which Astragalus polysaccharide nanoparticles (APS-CS/TPP) protect against septic myocardial injury, addressing the limited understanding of how APS-CS/TPP specific signaling pathways in this condition. Materials and Methods: Potential targets and pathways of Astragalus polysaccharide (APS) were initially predicted using network pharmacology, molecular docking, and microscale thermophoresis. APS-CS/TPP were prepared using an ion gel method with a chitosan derivative and characterized for formation, size, and surface charge. A murine model of septic myocardial injury was established by cecal ligation and puncture (CLP), and therapeutic outcomes were assessed via echocardiography, ELISA, histology, and Western blot. In vitro, H9c2 cells were stimulated with LPS and treated with APS-CS/TPP, with or without the HSP90AA1 inhibitor TAS-116, followed by evaluation of inflammatory markers and protein expression. Results: APS showed high binding affinity to HSP90AA1. APS-CS/TPP improved survival and attenuated myocardial damage in septic mice. In vitro, they reduced levels of IL-1β, IL-6, and TNF-α, and downregulated HSP90AA1, NLRP3, caspase-1, and IL-1β. These effects were suppressed by TAS-116. Conclusion: APS-CS/TPP protect against septic myocardial injury by inhibiting the HSP90AA1/NLRP3 signaling pathway. Keywords: nanoparticles, HSP90AA1, NLRP3, cardioprotection, astragalus polysaccharide

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Cite This Study

Yue et al. (Sun,) conducted a other in Male C57BL/6 mice aged 8-10 weeks with cecal ligation and puncture induced septic myocardial injury (n=82). Astragalus polysaccharide nanoparticles (APS-CS/TPP) vs. Saline gavage in sham and CLP control groups was evaluated on Survival rate at 72 hours after CLP, cardiac function measured by LVEF, LVFS, SV, CO at 8 hours post-CLP, myocardial injury assessed by histopathology and serum markers (cTnI, CK-MB, LDH) at 48 hours (Absolute improvement in survival by 23.34% (from 33.33% to 56.67%), p=<0.05). Astragalus polysaccharide nanoparticles (APS-CS/TPP) improved 72-hour survival by 23.3% and significantly restored cardiac function and reduced myocardial injury markers in septic mice compared to control.

synapsesocial.com/papers/699fe2eb95ddcd3a253e66d2 https://doi.org/https://doi.org/10.2147/ijn.s580840

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