Browse > Article
http://dx.doi.org/10.15616/BSL.2022.28.4.237

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 (Department of Biomedical Laboratory Science, Gwangju Health University)
Ji Seung Back (Department of Life Science, Chung-ang University)
Jae Hyun Jang (Department of Clinical Laboratory Science, Ansan University)
Abstract
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.
Keywords
5-iodo-6-amino-1,2-benzopyrone; ROS; Apoptosis; Hoechst 33342 assay; DCF-DA assay;
Citations & Related Records
연도 인용수 순위
  • Reference
1 Ha HC, Snyder SH. Poly(ADP-ribose) polymerase is a mediator of necrotic cell death by ATP depletion. Proc Natl Acad Sci USA. 1999. 96: 13978-13982.   DOI
2 He F, Wu Q, Xu B, Wang X, Wu J, Huang L, Cheng J. Suppression of Stim1 reduced intracellular calcium concentration and attenuated hypoxia/reoxygenation induced apoptosis in H9c2 cells. Biosci Rep. 2017. 37: BSR20171249.   DOI
3 Hochman JS, Choo H. Limitation of myocardial infarct expansion by reperfusion independent of myocardial salvage. Circulation. 1987. 75: 299-306.   DOI
4 Kalai T, Balog M, Szabo A, Gulyas G, Jeko J, Sumegi B, et al. New poly(ADP-ribose) polymerase-1 inhibitors with antioxidant activity based on 4-carboxamidobenzimidazole-2-ylpyrroline and -tetrahydropyridine nitroxides and -tetrahydropyridine nitroxides and their precursors. Journal of Medicinal Chemistry. 2009. 52: 1619-1629.   DOI
5 Lloyd-Jones D, Adams RJ, Brown TM, Carnethon M, Dai S, et al. Heart disease and stroke statistics--2010 update: a report from the American Heart Association. Circulation. 2010. 121: e46-e215.   DOI
6 Nanjo F, Goto K, Seto R, Suzuki M, Sakai M, Hara Y. Scavenging effects of tea catechins and their derivatives on 1,1-diphenyl-2-picrylhydrazyl radical. Free Radical Biology & Medicine. 1996. 21: 895-902.   DOI
7 Pacher P, Liaudet L, Mabley JG, Cziraki A, Hasko G, Szabo C. Beneficial effects of a novel ultrapotent poly(ADP-ribose) polymerase inhibitor in murine models of heart failure. International Journal of Molecular Medicine. 2006. 17: 369-375.
8 Park ES, Kang JC, Jang YC, Park JS, Jang SY, Kim DE, et al. Cardioprotective effects of rhamnetin in H9c2 cardiomyoblast cells under H(2)O(2)-induced apoptosis. Journal of Ethnopharmacology. 2014. 153: 552-560.   DOI
9 Pieper AA, Walles T, Wei G, Clements EE, Verma A, Snyder SH, et al. Myocardial postischemic injury is reduced by poly ADP ripose polymerase-1 gene disruption. Mol Med. 2000. 6: 271-282.   DOI
10 Pogue AI, Jones BM, Bhattacharjee S, Percy ME, Zhao Y, Lukiw WJ. Metal-sulfate induced generation of ROS in human brain cells: detection using an isomeric mixture of 5- and 6-carboxy-2',7'-dichlorofluorescein diacetate (carboxy-DCFDA) as a cell permeant tracer. Int J Mol Sci. 2012. 13: 9615-9626.   DOI
11 Powers SK, Lennon SL, Quindry J, Mehta JL. Exercise and cardioprotection. Curr Opin Cardiol. 2002. 17: 495-502.   DOI
12 Radnai B, Antus C, Racz B, Engelmann P, Priber JK, Tucsek Z, et al. Protective effect of the poly(ADP-ribose) polymerase inhibitor PJ34 on mitochondrial depolarization-mediated cell death in hepatocellular carcinoma cells involves attenuation of c-Jun N-terminal kinase-2 and protein kinase B/Akt activation. Mol Cancer. 2012. 11: 34.   DOI
13 Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction: pathophysiology and therapy. Circulation. 2000. 101: 2981-2988.   DOI
14 Sun L, Wang H, Yu S, Zhang L, Jiang J, Zhou Q. Herceptin induces ferroptosis and mitochondrial dysfunction in H9c2 cells. Int J Mol Med. 2022. 49: 17.
15 Szabo C. DNA strand breakage and activation of poly-ADP ribosyltransferase: a cytotoxic pathway triggered by peroxynitrite. Free Radic Biol Med. 1996. 21: 855-869.   DOI
16 Szabo C, Wong H, Bauer P, Kirsten E, Oconnor M, Zingarelli B, et al. Regulation of components of the inflammatory response by 5-iodo-6-amino-1,2-benzopyrone, an inhibitor of poly (ADP-ribose) synthetase and pleiotropic modifier of cellular signal pathways. Int J Oncol. 1997. 10: 1093-1101.   DOI
17 Zweier JL, Talukder MA. The role of oxidants and free radicals in reperfusion injury. Cardiovascular Research. 2006. 70: 181-190.   DOI
18 Tacar O, Sriamornsak P, Dass CR. Doxorubicin: an update on anticancer molecular action, toxicity and novel drug delivery systems. J Pharm Pharmacol. 2013. 65: 157-170.   DOI
19 Thiemermann C, Bowes J, Myint FP, Vane JR. Inhibition of the activity of poly(ADP ribose) synthetase reduces ischemiareperfusion injury in the heart and skeletal muscle. Proc Natl Acad Sci USA. 1997. 94: 679-683.   DOI
20 Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2003. 285: H579-588.   DOI
21 Endres M, Scott GS, Salzman AL, Kun E, Moskowitz MA, Szabo C. Protective effects of 5-iodo-6-amino-1,2-benzopyrone, an inhibitor of poly(ADP-ribose) synthetase against peroxynitrite-induced glial damage and stroke development. Eur J Pharmacol. 1998. 351: 377-382.   DOI
22 Aikawa R, Nawano M, Gu Y, Katagiri H, Asano T, Zhu W, et al. Insulin prevents cardiomyocytes from oxidative stress-induced apoptosis through activation of PI3 kinase/Akt. Circulation. 2000. 102: 2873-2879.   DOI
23 Cave A, Garlick P. Re: Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. J Mol Cell Cardiol. 2000. 32: 1759-1760.   DOI
24 Crowley LC, Marfell BJ, Waterhouse NJ. Analyzing cell death by nuclear staining with Hoechst 33342. Cold Spring Harb Protoc. 2016. 2016.
25 Chen CF, Wang D, Hwang CP, Liu HW, Wei J, Lee RP, et al. The protective effect of niacinamide on ischemia-reperfusion-induced liver injury. Journal of Biomedical Science. 2001. 8: 446452.
26 Cuzzocrea S, Riley DP, Caputi AP, Salvemini D. Antioxidant therapy: a new pharmacological approach in shock, inflammation, and ischemia/reperfusion injury. Pharmacological Reviews. 2001. 53: 135-159.
27 Franson RC, Rosenthal MD, Regelson W. Mechanism(s) of cytoprotective and anti-inflammatory activity of PGB1 oligomers: PGBx has potent anti-phospholipase A2 and anti-oxidant activity. Prostaglandins Leukot Essent Fat Acids. 1991. 43: 63-70.   DOI
28 Flaherty JT, Zweier JL. Role of oxygen radicals in myocardial reperfusion injury: experimental and clinical evidence. Klinische Wochenschrift. 1991. 69: 1061-1065.
29 Giansanti V, Dona F, Tillhon M, Scovassi AI. PARP inhibitors: new tools to protect from inflammation. Biochemical Pharmacology. 2010. 80: 1869-1877.   DOI
30 Gilad E, Zingarelli B, Salzman AL, Szabo C. Protection by inhibition of poly(ADP-ribose) synthetase against oxidant injury in cardiac myoblasts In vitro. Journal of Molecular and Cellular Cardiology. 1997. 29: 2585-2597.   DOI