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作 者:赵莉莉[1] 黄元伟[1] 但青宏[1] 孙坚[1] 朱朝晖
机构地区:[1]浙江医科大学附属第一医院心内科
出 处:《浙江医科大学学报》1998年第6期248-251,共4页
摘 要:目的:研究人单纯疱疾病毒1型(HSV-1)对血管平滑肌细胞(SMC)脂质代谢的影响,探讨HSV一且与动脉粥样硬化(AS)的关系。方法;以HSV-1感染体外培养的牛主动脉平滑肌细胞,观察细胞形态和超微结构的改变,以及细胞内脂质代谢的变化。结果:HSV-1感染后,用PCR法能检出SMC内存在HSV-1核酸片段;感染后24h和36h,感染组细胞内总胆固醇(CH)较对照组明显增高(P<0.05),HE染色和电镜下均显示感染组细胞空泡样变。结论:HSV-1不但能在体外感染血管SMC,且能导致SMC内胆固醇积聚,可能促使SMC向SMC源性泡沫细胞转变,从而参与动脉粥样硬化的发病过程。Objective:To investigate the effects of human herpes simplex virus type 1 (HSV-1 )infection on morphology, ultrastructure and lipid metabolism in vascular smooth muscle cells (SMC),exploring the possible role of HSV-1 in the etiology of atherosclerosis(AS) on cell level. Methods: Bovine aortic SMC in culture were infectedwith HSV-1. The change of morphology, ultrastructure and lipid metabolism in infected SMC was examined.Results: (1)HSV-1 nucleic acids were detected in infected SMC by PCR. (2)At 24 h and 36 h after infection,the cellular cholesterol concentration of the infected groups significantly increased compared with that of the uninfected groups(p<0. 05). (3)HE straining and transmission electron microscope observed the appearance of numerous intracellular vacuoles in the infected SMC. Conclusion: HSV-1 can infect vascular SMC in vitro. It also can cause lipid, especially cholesterol accumulation in SMC. Furthermore, cultured SMC may change to SMC derived foam cells after HSV-1 infection. All this strongly supports the hypothesis that HSV-1 is involved in the pathogenesis of AS and may play a causative role in AS.
分 类 号:R543.502[医药卫生—心血管疾病] R373.11[医药卫生—内科学]
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