Arquivos brasileiros de cardiologia · 2026
Astragalus Polysaccharide Enhances Mitochondrial Biogenesis and Function in Cardiomyocytes Through AMPK Activation.
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Wang Chengbin, Lv Shuhan, Liu Xingde
Аннотация
BACKGROUND: Mitochondrial dysfunction is a key driver of heart failure, underscoring the need for therapies that promote mitochondrial biogenesis and function. Astragalus polysaccharide (APS), a bioactive compound from Astragalus membranaceus, has demonstrated cardioprotective properties, but its direct effects on mitochondrial homeostasis in cardiomyocytes remain unclear.
OBJECTIVES: This study aimed to investigate the effects of APS on mitochondrial function and biogenesis in HL-1 cardiomyocytes and to elucidate the involvement of the AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) signaling pathway.
METHODS: HL-1 cardiomyocytes were treated with non-toxic concentrations of APS (1.25-2.5 g/L) for 48 hours. Mitochondrial respiration was assessed via Seahorse XF Analyzer, adenosine triphosphate (ATP) levels were quantified, and Complex IV activity was measured. Mitochondrial biogenesis was evaluated by mitochondrial DNA (mtDNA)/ nuclear DNA (nDNA) ratio, cytochrome B levels, and mitochondrial mass. Key proteins and genes, including PGC-1α, nuclear respiratory factor 2 (NRF2), mitochondrial transcription factor A (TFAM), uncoupling protein 2 (UCP2), and phosphorylated AMPK (p-AMPK), were analyzed by Western blot and qPCR. The AMPK inhibitor Compound C was used to confirm the pathway's role.
RESULTS: APS treatment significantly enhanced mitochondrial respiration, ATP production, and Complex IV activity. It promoted mitochondrial biogenesis, evidenced by increased mtDNA/nDNA ratio and mitochondrial mass. APS upregulated the expression of PGC-1α, NRF2, TFAM, and UCP2, and activated AMPK phosphorylation. All these beneficial effects were abolished by AMPK inhibition with Compound C.
CONCLUSIONS: APS enhances mitochondrial biogenesis and function in cardiomyocytes through activation of the AMPK/PGC-1α signaling pathway, identifying it as a potential therapeutic agent for cardiac diseases associated with mitochondrial dysfunction.
OBJECTIVES: This study aimed to investigate the effects of APS on mitochondrial function and biogenesis in HL-1 cardiomyocytes and to elucidate the involvement of the AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) signaling pathway.
METHODS: HL-1 cardiomyocytes were treated with non-toxic concentrations of APS (1.25-2.5 g/L) for 48 hours. Mitochondrial respiration was assessed via Seahorse XF Analyzer, adenosine triphosphate (ATP) levels were quantified, and Complex IV activity was measured. Mitochondrial biogenesis was evaluated by mitochondrial DNA (mtDNA)/ nuclear DNA (nDNA) ratio, cytochrome B levels, and mitochondrial mass. Key proteins and genes, including PGC-1α, nuclear respiratory factor 2 (NRF2), mitochondrial transcription factor A (TFAM), uncoupling protein 2 (UCP2), and phosphorylated AMPK (p-AMPK), were analyzed by Western blot and qPCR. The AMPK inhibitor Compound C was used to confirm the pathway's role.
RESULTS: APS treatment significantly enhanced mitochondrial respiration, ATP production, and Complex IV activity. It promoted mitochondrial biogenesis, evidenced by increased mtDNA/nDNA ratio and mitochondrial mass. APS upregulated the expression of PGC-1α, NRF2, TFAM, and UCP2, and activated AMPK phosphorylation. All these beneficial effects were abolished by AMPK inhibition with Compound C.
CONCLUSIONS: APS enhances mitochondrial biogenesis and function in cardiomyocytes through activation of the AMPK/PGC-1α signaling pathway, identifying it as a potential therapeutic agent for cardiac diseases associated with mitochondrial dysfunction.