International journal of biological macromoleculesNov 25, 2019

Astragalus polysaccharide nanoparticles may protect the heart during sepsis by blocking an immune signaling pathway

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 4, 2026

Abstract

Treatment with astragalus polysaccharide (APS) nanoparticles significantly reduced cardiac troponin I levels in a mouse model of sepsis-induced myocardial injury.

APS nanoparticles maintained cell viability and morphology while exhibiting anti-apoptotic effects in LPS-treated heart cells.
In animal studies, APS nanoparticles attenuated sepsis-induced myocardial injury by reducing bacterial loads and serum inflammatory markers.
Treatment with APS nanoparticles alleviated myocardial histopathologic abnormalities in mice.
The use of APS nanoparticles significantly decreased the expression of inflammatory cytokines in the heart.
The protective mechanism of APS nanoparticles is associated with the suppression of the TLR4/NF-κB signaling pathway.

Simplified

Sepsis-induced myocardial dysfunction was the leading cause of morbidity and mortality in hospitalized patients and yet there were no effective therapies. With excessive released inflammatory mediators through the TLR4-trigger NF-κB signaling pathway being implicated as key players in sepsis-induced myocardial injury, we prepared astragalus polysaccharide (APS) nanoparticles as an TLR4-responsive drug for alleviating sepsis-induced myocardial injury. Firstly, treatment with APS nanoparticles in LPS-treated H9c2 cells to evaluate the direct effect demonstrated that this drug maintained the cell viability, cell morphology and exerted anti-apoptotic effects. Additionally, animal studies using cecal ligation and puncture (CLP) in C57BL/6 mice revealed that APS nanoparticles were much more efficacious in attenuating sepsis-induced myocardial injury by down-regulating the bacterial loads, inhibiting serum C-reactive protein (CRP), white blood cells (WBC) levels, alleviating myocardial histopathologic abnormalities, remarkably reducing the cardiac troponin I (cTnI). Moreover, APS nanoparticles significantly decreased the myocardial inflammatory cytokine expression and inhibited the activity of TLR4/NF-κB pathway. In conclusion, APS nanoparticles could protect the sepsis-induced cardiac dysfunction. The mechanism of the protective action of APS nanoparticles seems to involve its ability to reduce inflammatory response and to suppress TLR4/NF-κB pathway. This drug may be a potential candidate strategy for septic cardiac dysfunction treatment.

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Declaration of Competing Interest All the authors declare no conflicts of interest. There was not any prior presentation of abstracts at meetings regarding the research.

PubMed

Astragalus polysaccharide nanoparticles may protect the heart during sepsis by blocking an immune signaling pathway

Abstract

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Abstract

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