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Arozal W., Watanabe K., Veeraveedu P.T., Ma M., Nafrialdi
32067462200;55492737200;12796732500;7202444988;8521176100;
Telmisartan inhibits the progression of cardiomyopathy in daunorubicin treated rats: The role of advanced glycation end products
2011
Medical Journal of Indonesia
20
4
255
262
1
Department of Pharmacology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia; Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata City, Japan
Arozal, W., Department of Pharmacology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia, Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata City, Japan; Watanabe, K., Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata City, Japan; Veeraveedu, P.T., Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata City, Japan; Ma, M., Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata City, Japan; Nafrialdi, Department of Pharmacology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia
Background: Anthracyclines have been reported to induce cardiotoxicity through mechanisms involving formation of advanced glycation end-products (AGEs), including pentosidine and Nє-(carboxymethyl) lysine (CML). We investigated the potential utility of telmisartan (TML), an angiotensin II receptor antagonists (ARB) on anthracycline-induced cardiotoxicity. Methods: Three groups of Sprague-Dawley rats were treated as follows: The first group received daunorubicin (DNR) 3 mg/kgBW every alternating day to reach a cumulative dose of 9 mg/kg DNR. The second group received DNR plus TLM at a dose10 mg/kgBW, by oral gavage for 6 weeks, and the third group served as control group (CTL) which only received vehicle of DNR. Mean blood pressure (MBP) peak left ventricular pressure (LVP), LV end-diastolic pressure (LVEDP), and intra-ventricular contractility (±dP/dt) were recorded by using Powerlab instrumentation. Ejection fraction (EF), and fractional shortening (FS) were measured by echocardiography. Expression of receptor of AGE (RAGE), pentosidine and CML were measured by immunohistochemistry and Western blot in LV tissue. Results: DNR treatment was associated with significant weakening of some hemodynamic parameters which could be reversed by TML (LVP: 124.3 ± 6.0; 111 ± 7; and 115.1 ± 5.4 mmHg, respectively in CTL, DNR and DNR-TLM groups; LVEDP: 7.5 ± 0.9; 10.7 ± 0.3; 8.7 ± 0.4 mmHg, respectively; +dP/dt: 6813 ± 541; 4800 ± 345; 5950 ± 398 mmHg/s, respectively). The same phenomenons were also observed on echocardiographic parameters (EF: 78.9 ± 1.8; 59.6 ± 1.4; 76.2 ± 2.75%, resepectively; FS: 42.8 ± 1.7; 29.1 ± 1.3; 41 ± 2.7%) respectively. Expression of RAGE as well as pentosidine and CML were increased in DNR-rats. TML treatment ameliorated these changes. Conclusion: These results suggested the role of AGE formation in DNR-induced cardiotoxicity and telmisartan could inhibit the progression of cardiac toxicity at least in part by reduction RAGE expressiom. © (Publication Year), (publisher Name). All rights reserved.
Advanced glycation end product; Anthracyline; Cardiotoxicity; Daunorubicin; Telmisartan
6 n carboxymethyllysine; advanced glycation end product; advanced glycation end product receptor; daunorubicin; pentosidine; telmisartan; animal model; animal tissue; Article; cardiomyopathy; cardiotoxicity; controlled study; disease course; drug efficacy; drug mechanism; fractional shortening; heart ejection fraction; heart left ventricle enddiastolic pressure; heart left ventricle pressure; heart muscle injury; heart ventricle contractility; heart weight; histopathology; immunohistochemistry; male; mean arterial pressure; nonhuman; rat; two dimensional echocardiography; Western blotting
Faculty of Medicine, Universitas Indonesia
08531773
Article
Q3