• Lingling Qi, Huanjun Pan, Dongye Li, Fang Fang, Dan Chen, and Hong Sun.
• Institute of Cardiovascular Disease Research, Xuzhou Medical College Affiliated Hospital, China.
• Eur. J. Pharmacol. 2011 Oct 1; 668 (1-2): 201-7.

AbstractLuteolin occurs in a variety of plants and possesses antioxidant and anti-inflammatory properties. However, its role in protection against ischemia-reperfusion injury in Sprague-Dawley rats has not been elucidated. In the present study, we tested the contractile function of left ventricular cardiomyocytes with different concentrations of luteolin: 0.5, 1.5, 2.5 and 5.0 μg/ml after simulated. We investigated the direct effect of luteolin against necrosis and apoptosis following ischemia-reperfusion in cardiomyocytes. We further observed the function of isolated hearts subjected to ischemia-reperfusion with or without 10.0 μg/ml luteolin pretreatment. Following 24h incubation with or without luteolin, adult rat cardiomyocytes were subjected to 3h of ischemia followed by 2h of reperfusion for contractile function and necrosis (trypan blue exclusion and lactate dehydrogenase release) or 18 h of reperfusion for apoptosis studies. The cardiomyocyte shortening amplitude depended on different concentrations of luteolin, increasing significantly at 2.5 μg/ml luteolin (P<0.01). Necrosis and apoptosis were reduced by luteolin at 2.5 μg/ml. In addition, the expression of Bcl-2 was upregulated by luteolin and the ratio of Bax to Bcl-2 was decreased. Luteolin inhibited the activation of Caspase3 after ischemia-reperfusion in cardiomyocytes. Furthermore, luteolin at 10.0 μg/ml improved ischemia-reperfusion induced myocardial function, by improving heart rate, +dp/dt(max) and -dp/dt(max), and also limiting the decline of left ventricular systolic pressure (LVSP) and elevation of left ventricular end-diastolic pressure (LVEDP) to some extent. Our results demonstrated that luteolin prevents ischemia-reperfusion injury by reducing necrosis and apoptosis in rat cardiomyocytes.Copyright © 2011 Elsevier B.V. All rights reserved.

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