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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.