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, 2004?and?Sanz-Rosa et al., 2005). The increased activity of these pathways prompted us to evaluate whether the infliximab-induced changes in AKT/eNOS pathway were associated with modulation of inflammatory pathways. Our data demonstrated that JNK phosphorylation was 143% higher in the aortas of rats in the SHR+veh group compared to the aortas of rats in the WKY+veh group (P[http://www.selleckchem.com/products/Imatinib-Mesylate.html Imatinib solubility dmso] The phosphorylation [http://www.selleckchem.com/products/VX-770.html www.selleckchem.com/products/VX-770.html] levels of I�ʦ�, a direct target of I��K, were not significantly different when comparing the aortas of WKY+veh rats to those of SHR+veh rats. Treatment with infliximab reduced the phosphorylation of I�ʦ� in the aortas of rats in the SHR+inflix 1.5 and SHR+inflix 6 groups (to 48% and 42% of SHR+veh values, respectively; P[https://en.wikipedia.org/wiki/Oxymatrine Oxymatrine] caused by infliximab (Anker and Coats, 2002), we next investigated the cardiac tissue of WKY and SHR treated with either vehicle or infliximab. Echocardiography of untreated and infliximab-treated WKY and SHR rats (8 weeks of treatment) revealed no differences in heart rate, ejection fraction and left-ventricular end-systolic and end-diastolic diameters at different infliximab doses. Although its effect was not dose dependent, infliximab reduced end-diastolic septal wall thickness, end-diastolic posterior wall thickness, relative wall thickness, left ventricle mass and left ventricle mass index in SHR. Consistent with this echocardiographic finding, histometric analysis showed that infliximab reduced the diameters of cardiomyocytes in SHR.