Title: Selective inhibition of p38α mitogen-activated protein kinase improves cardiac function and reduces myocardial apoptosis in rat model of acute myocardial injury induced by L-NAME/angiotensin II
Abstract: p38 mitogen-activated protein kinase (MAPK) is activated during heart disease. However, whether p38 MAPK inhibition is cardioprotective still remain unclear. In a model of acute myocardial injury induced by Nω-nitro-L-arginine methyl ester (L-NAME)/angiotensin II (Ang II), we investigated the cardioprotective effects of selective p38α MAPK inhibition using a synthesized inhibitor, SD-282. Rats were treated with L-NAME (40 mg/kg/day) in drinking water plus 1% salt for 14 days along with Ang II (0.5 mg/kg/day) for 3 days. SD-282 (60 mg/kg) was administrated orally, twice a day for 4 days, starting a day prior to Ang II administration. The cardioprotective effects of p38α MAPK inhibition were evaluated by improvement of cardiac function, reduction of inflammatory cell infiltration and cardiomyocytes apoptosis. It demonstrated that the p38α MAPK inhibitor, SD-282 improved cardiac function indicated by increase in stroke volume (SV), cardiac output (CO), ejection fraction (EF), stroke work (SW) and decrease in arterial elastance (Ea). (Table) Tabled 1 Cardiac Function of Rats Treated With or Without SD-282 Group HR (bpm) SV (ul) CO (ul/min) EF (%) SW (mmHg∗ul) Ea (mmHg/ul) n Control 340±27 8.5±0.8 2902±314 30.5±1.5 677.7±47.5 17.1±1.8 6 Vehicle 269±30 3.1±1.1 766±265 14.4±3.5 276.4±181 55.4±16.4 9 SD-282 284±14 6.5±2.6 1831±723 21.6±6.8 549.8±274 29.5±19.6 9 p value ns <0.01 <0.001 <0.01 <0.001 <0.001 Open table in a new tab
Publication Year: 2004
Publication Date: 2004-08-01
Language: en
Type: article
Indexed In: ['crossref']
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