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 μg·mL-1) for 4 h and treated with AS IV at 50, 100, and 150 μmol·L-1 for various durations. Cell viability was determined by MTT. The content of released TNF-α 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 mR NA and protein expression levels of NF-κB p65 were measured by RT-PCR and Western blotting, respectively. And the NF-κB p65 activity was measured by ELISA. Our results demonstrated that AS IV at 50, 100, and 150 μmol·L-1 markedly inhibited the release of TNF-α and IL-6 and decreased NF-κB 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. 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 μg · mL-1) for 4 h and treated with AS IV at The content of released TNF-α and IL-6 from cardiomyocytes were evaluated by enzyme-linked immunosorbent assay (ELISA). The levels of 50, 100, and 150 μmol·L-1 for various durations. Cell viability was determined by MTT. The mR NA and protein expression levels of NF-κB p65 were measured by RT-PCR, and the activity of superoxide dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH), and creatine phosphate kinase (CK) were measured by using commercial available kits And the NF-κB p65 activity was measured by ELISA. Our results for that AS IV at 50, 100, and 150 μmol·L-1 markedly inhibited the release of TNF-α and IL-6 NF-κB expression, compared with the model group. Moreover, the improved SOD ac 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 act that AS IV could prevent LPS-induced injury in cardiomyocytes.