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(P<0.001);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。
Objective To explore the role of lipid rafts in coxsackievirus B3 (CVB3)-infected cardiocytes. Methods Methyl-β-cyclodextrin(Ml3CD) was used to remove the cholesterol molecules maitaining the stability of lipid rafts on cell membrane,then the cells were infected with CVB3;western blot was adopted to detect the expression of CVB3 VP1 protein. Virus titer was determined after adding exogenous choleserol to observe inhibitive effect of MβCD on CVB3 infection. Resdts The damage of cell membrane lipid rafts duo to the removement of the cholesterol molecules by MβCD could inhibit the in- fection of CVB3 to cells and reduce the virus titer,and exogenous cholesterol could regain the inhibition of MβCD to CVB3 infection. Conclusion The lipid rafts on cardiocytes membrane plays an important role in CVB3 infection to the host cell.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2013年第2期228-229,共2页
Chinese Journal of Public Health
基金
吉林省科技厅资助项目(200905181)
吉林省卫生厅资助项目(2010Z051)