We have established a novel photochemical model of intimal thickening in the rat femoral artery. The endothelium was injured by the photochemical reaction between rose bengal and green light, which was followed by thrombotic occlusion, vascular smooth muscle cells (VSMC) migration and proliferation. The neointima was formed by proliferated VSMC and the extracellular matrix, reaching to maximal thickness within 3 weeks after the endothelial injury. Using this model, we have investigated the effect of several anti-proliferative drugs, anti-allergic drugs, angiotensin converting enzyme inhibitors, prostaglandin E1, anti-thrombotics, or leukotrienes receptor antagonists, on intimal thickening. This model has two major advantages in comparison with other methods: one is that the media is free from mechanical stress, and the model is expected to represent pathological changes close to clinical atherosclerosis. Another advantage is that this method is also applicable to small animals such as mice, including transgenic mice. These advantages are very helpful for investigating the mechanism of atherogenesis.
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