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The proliferation and migration of vascular smooth muscle cells (VSMCs) are critical events in the pathogenesis of atherosclerosis and hypertension. Naringenin inhibited TNF-α–induced VSMC proliferation and migration in a dose-dependent manner . It also blocked the increased reactive oxygen species (ROS) generation induced by TNF-α. Oxidative stress and TNF-α may also trigger the activation of mitogen-activated protein kinases (MAPKs), which are the key regulatory factors for VSMC proliferation. Naringenin prevented extracellular signal–regulated kinase (ERK)/MAPK and Akt phosphorylation, whereas p38 MAPK and c-Jun N-terminal kinases (JNKs) were unchanged. This overall effect is probably mediated via the induction of heme oxygenase 1 (HO-1) and reduction in oxidative stress.
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