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Mechanisms of atherosclerosis caused by arsenic exposure in animal model

机译:动物模型中砷暴露引起的动脉粥样硬化机制

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Chronic arsenic (As) exposure causing increase incident of cardiovascular and cerebrovascular diseases had been demonstrated by many epidemiological studies (Guo et al., 2001; Tseng et al., 2003; Watanabe et al., 2001). Recently, a few clinical and animal studies presented that atherosclerosis was one of the most important causes to increase the risk of cardiovascular disease or cerebrovascular disease (Bots et al., 1997; Chambless et al., 1997; Mertens & Holvoet, 2001; O'Leary et al., 1999) and could be a possible cause after chronic As exposure. However, the exact mechanisms are currently under debate. Several reports suggested that the high-cholesterol diet (HCD) resulted in hypercholesterolemia inducing atherosclerosis and many heavy metals were possibly susceptible to HCD-induced atherosclerosis. However, the exact mechanisms of atherosclerosis induced by chronic As exposure either alone or in combination with HCD are currently still unclear. An animal model was set up to evaluate the mechanisms of As-induced atherosclerosis in association with HCD administration.
机译:造成事故增加心脑血管疾病的慢性砷(As)曝光已经被许多流行病学研究表明(Guo等,2001;曾雅妮等,2003; Watanabe等,2001)。最近,一些临床和动物研究表明,动脉粥样硬化是增加心血管疾病或脑血管病风险的最重要原因之一(BOTS等,1997; Chambless等,1997; Mertens&Holvoet,2001; o 'Leary等,1999)并且可能是慢性曝光后可能的原因。但是,确切的机制目前正在辩论中。一些报道表明,高胆固醇饮食(HCD)导致高胆固醇血症诱导动脉粥样硬化,许多重金属可能易于HCD诱导的动脉粥样硬化。然而,目前尚不清楚,慢性为单独或与HCD组合诱导的动脉粥样硬化的确切机制目前尚不清楚。设立了一种动物模型,以评估与HCD给药相关​​的诱发动脉粥样硬化的机制。

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