• Title/Summary/Keyword: 5-iodo-6-amino-1,2-benzopyrone

Search Result 1, Processing Time 0.019 seconds

The Preventive Effect of 5-Iodo-6-Amino-1,2-Benzopyrone on Apoptosis of Rat Heart-derived Cells induced by Oxidative Stress

  • Kyoumg A Chung;Ji Seung Back;Jae Hyun Jang
    • Biomedical Science Letters
    • /
    • v.28 no.4
    • /
    • pp.237-246
    • /
    • 2022
  • Ischemia-reperfusion results in excess reactive oxygen species (ROS) that affect myocardial cell damage. ROS production inhibition is effectively proposed in treating cardiovascular diseases including myocardial hypertrophy. Studies have shown that oxidizing cultured cells in in vitro experiments gradually decreases the permeability of mitochondrial membranes time- and concentration-dependent, resulting in increased mitochondrial membrane damage due to secondary ROS production and cardiolipin loss. However, recent studies have shown that 5-iodo-6-amino-1,2-benzopyrone (INH2BP), an anticancer and antiviral drug, inhibited peroxynitrite-induced cell damage in in vitro and alleviated partial or overall inflammation in animal experiments. Therefore, in this paper, we studied the preventive effect of INH2BP on H9c2 cells derived from mouse heart damaged by oxidative stress using 700 μM of hydrogen peroxide. As a result of oxidative stress to H9c2 cells by hydrogen peroxide whether the treatment of INH2BP or not, hydrogen peroxide caused serious damage in H9c2 cells. These results were confirmed with cell viability and Hoechst 33342 assays. And this damage was through cell death. However, it was confirmed that H9c2 cells pretreated with INH2BP significantly reduced cell death by hydrogen peroxide. In addition, measurements with DCF-DA assay to determine whether ROS is produced in H9c2 cells treated with only hydrogen peroxide produced ROS significantly, but H9c2 cells pretreated with INH2BP significantly reduced ROS production by hydrogen peroxide. Taken together, it is believed that INH2BP can be useful for the prevention and treatment of cardiovascular diseases induced through oxidative stress such as heart damage caused by ischemia/reperfusion.