Telmisartan inhibits the progression of cardiomyopathy in daunorubicin treated rats: the role of advanced glycation end products  

Oleh:

Arozal, Wawaimuli ; Watanabe, Kenichi ; Veeraveedu, Punniyakoti T. ; Ma, Meilei ; Nafrialdi

Jenis: Article from Journal - ilmiah nasional - terakreditasi DIKTI
Dalam koleksi: Medical Journal of Indonesia vol. 20 no. 04 (Nov. 2011), page 255-262.
Fulltext: Volume 20, Issue 4, November 2011 - Telmisartan inhibits the progression of cardiomyopathy in daunorubicin treated rats- the role of advanced glycation end products .pdf (1.21MB)

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Perpustakaan FK Nomor Panggil: M35.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Background: Anthracyclines have been reported to induce cardiotoxicity through mechanisms involving formation of advanced glycation end-products (AGEs), including pentosidine and N?-(carboxymethyl) lysine (CML). We investigated the potential utility of telmisartan (TML), an angiotensin II receptor antagonists (ARB) on anthracycline-induced cardiotoxicity. Method: Three groups of Sprague-Dawley rats were treated as follows: The first group received daunorubicin (DNR) 3 mg/kgBW (via caudal vein) 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. Hemodynamic parameters {mean blood pressure (MBP), peak left ventricular pressure (LVP), LV end-diastolic pressure (LVEDP), and the rate of intra-ventricular pressure rise and decline (±dP/dt)} were recorded by using Powerlab instrumentation. While left ventricular dimension (systolic and diastolic, LVDs,LVDd), 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. Histopathological examination were performed by Hematoxillin-Eosin and Azan-Malory staining. Statistical analysis was done by ANOVA. Results DNR treatment was associated with significant weakening of some hemodynamib parameters which could be reserved 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 alteration of AGE formation through their receptor, RAGE.

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