脂筏在柯萨奇B3病毒感染心肌细胞中作用

发布时间：2018-06-10 03:14

本文选题：脂筏 + 甲基-β-环糊精(MβCD)　；参考：《中国公共卫生》2013年02期

【摘要】：目的探讨脂筏在柯萨奇B3病毒(CVB3)感染心肌细胞中的作用,旨在为阐明CVB3致病的分子机理及寻找新的抗病毒靶点提供依据。方法用甲基-β-环糊精(MβCD)去除细胞膜维持脂筏稳定性的胆固醇分子后感染CVB3,用Western blot法检测CVB3 VP1蛋白的表达并测定病毒的滴度,同时观察补充外源性胆固醇恢复MβCD对CVB3感染的抑制作用。结果用MβCD去除胆固醇分子破坏细胞膜脂筏结构,可抑制CVB3感染细胞;1.2、5.5和10 mmol/L MβCD去除细胞膜胆固醇CVB3滴度分别为(4.2±0.06)、(3.5±1.05)、(3.0±0.15)和(2.0±0.15)lgP-FU/mL,均低于无MβCD处理对照组的(5.7±0.06)lgPFU/mL(P0.001);补充外源性胆固醇可恢复MβCD对CVB3感染的抑制作用。结论细胞膜脂筏在CVB3感染心肌细胞中起重要作用,是病毒进入细胞的关键因素。
[Abstract]:Objective to investigate the role of lipid rafts in cardiomyocytes infected with Coxsackie B _ 3 virus CVB _ 3 in order to elucidate the molecular mechanism of CVB _ 3 and find new antiviral targets. Methods Methyl- 尾 -cyclodextrin M 尾 CDD was used to remove cholesterol molecules which maintained the stability of lipid rafts and then infected with CVB3. The expression of VP1 protein and the titer of virus were detected by Western blot assay. At the same time, the inhibitory effect of supplementation of exogenous cholesterol on CVB 3 infection was observed. Results cholesterol molecules were removed by M 尾 CD to destroy membrane lipid raft structure. The titers of cholesterol CVB3 were 4.2 卤0.06, 3.5 卤1.05 卤0.15 and 2.0 卤0.15lgP-FUmLrespectively, which were lower than those of control group (5.7 卤0.06lgPFUmLP0.001), and the inhibitory effect of M 尾 CD on CVB3 infection was recovered by supplementation of exogenous cholesterol. Conclusion membrane lipid raft plays an important role in CVB 3 infection of cardiomyocytes and is a key factor for virus entry into cardiomyocytes.
【作者单位】：吉林大学白求恩医学院病原生物学教研室;日本筑波大学医学部;
【基金】：吉林省科技厅资助项目(200905181) 吉林省卫生厅资助项目(2010Z051)
【分类号】：R363

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