Inhibitory Effects of Astragalus Polysaccharide on Myocardial Apoptosis Induced by Hypoxia or Reoxygenation in Rats

Abstract

To explore the inhibitory effects of Astragalus polysaccharide on myocardial apoptosis induced by hypoxia/ reoxygenation in rats based on the high mobility group box 1/toll-like receptor 4/nuclear factor kappa B signaling pathway. The hypoxia/reoxygenation injury model of H9C2 myocardial cells was established and divided into control group, hypoxia/reoxygenation group, Astragalus polysaccharide group and high mobility group box 1 inhibitor group. Cell proliferation and apoptosis were detected by cell counting kit-8 assay and Annexin V-fluorescein isothiocyanate/propidium iodide double staining. The messenger RNA expressions of high mobility group box 1, toll-like receptor 4 and nuclear factor kappa B were detected by quantitative reverse transcription polymerase chain reaction and the contents of tumor necrosis factor alpha, interleukin-1β and interleukin-6 were determined using enzyme-linked immunosorbent assay. Compared with control group, cell proliferation was significantly weakened, apoptosis was significantly enhanced and the messenger RNA expressions of high mobility group box 1, toll-like receptor 4 and nuclear factor kappa B and the contents of tumor necrosis factor alpha, interleukin-1β and interleukin-6 significantly increased in hypoxia/reoxygenation group (p<0.05). Compared with hypoxia/reoxygenation group, Astragalus polysaccharide group and high mobility group box 1 inhibitor group had significantly enhanced cell proliferation, weakened apoptosis and decreased messenger RNA expressions of high mobility group box 1, toll-like receptor 4 and nuclear factor kappa B and contents of tumor necrosis factor alpha, interleukin-1β and interleukin-6 (p<0.05). Astragalus polysaccharide can repair the hypoxia/ reoxygenation injury of H9C2 myocardial cells, which may suppress apoptosis through inhibiting the high mobility group box 1/toll-like receptor 4/nuclear factor kappa B signaling pathway.