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Astragaloside IV prevents lipopolysaccharide-induced injury in H9C2 cardiomyocytes

Astragaloside IV prevents lipopolysaccharide-induced injury in H9C2 cardiomyocytes

  • 摘要: This study aimed to investigate the protective effects of astragaloside IV (AS IV) on lipopolysaccharide (LPS)-induced injury in H9C2 cardiomyocytes. H9C2 Cardiomyocytes were cultured with LPS (10 gmL-1) for 4 h and treated with AS IV at 50, 100, and 150 molL-1 for various durations. Cell viability was determined by MTT. The content of released TNF- and IL-6 from cardiomyocytes were evaluated by enzyme-linked immunosorbent assay (ELISA). The levels of superoxidase dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH), and creatine phosphate kinase (CK) were measured by using commercial available kits. The mRNA and protein expression levels of NF-B p65 were measured by RT-PCR and Western blotting, respectively. And the NF-B p65 activity was measured by ELISA. Our results demonstrated that AS IV at 50, 100, and 150 molL-1 markedly inhibited the release of TNF- and IL-6 and decreased NF-B expression, compared with the model group. Moreover, the improved SOD activity and decreased MDA, LDH and CK levels were detected after AS IV treatment. In summary, AS IV could increase the activities of antioxidant enzymes, inhibite lipid peroxidation, and down-regulate the inflammatory mediators involved in the inflammatory responses. These results demonstrated that AS IV could prevent LPS-induced injury in cardiomyocytes.

     

    Abstract: This study aimed to investigate the protective effects of astragaloside IV (AS IV) on lipopolysaccharide (LPS)-induced injury in H9C2 cardiomyocytes. H9C2 Cardiomyocytes were cultured with LPS (10 gmL-1) for 4 h and treated with AS IV at 50, 100, and 150 molL-1 for various durations. Cell viability was determined by MTT. The content of released TNF- and IL-6 from cardiomyocytes were evaluated by enzyme-linked immunosorbent assay (ELISA). The levels of superoxidase dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH), and creatine phosphate kinase (CK) were measured by using commercial available kits. The mRNA and protein expression levels of NF-B p65 were measured by RT-PCR and Western blotting, respectively. And the NF-B p65 activity was measured by ELISA. Our results demonstrated that AS IV at 50, 100, and 150 molL-1 markedly inhibited the release of TNF- and IL-6 and decreased NF-B expression, compared with the model group. Moreover, the improved SOD activity and decreased MDA, LDH and CK levels were detected after AS IV treatment. In summary, AS IV could increase the activities of antioxidant enzymes, inhibite lipid peroxidation, and down-regulate the inflammatory mediators involved in the inflammatory responses. These results demonstrated that AS IV could prevent LPS-induced injury in cardiomyocytes.

     

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