中华实验和临床病毒学杂志
中華實驗和臨床病毒學雜誌
중화실험화림상병독학잡지
CHINESE JOURNAL OF EXPERIMENTAL AND CLINICAL VIROLOGY
2010年
6期
433-435
,共3页
易立%王佳伟%赵日光%脱厚珍%冯子敬%王得新
易立%王佳偉%趙日光%脫厚珍%馮子敬%王得新
역립%왕가위%조일광%탈후진%풍자경%왕득신
鼠巨细胞病毒属%动脉硬化%小鼠%氟伐他汀
鼠巨細胞病毒屬%動脈硬化%小鼠%氟伐他汀
서거세포병독속%동맥경화%소서%불벌타정
Muromegalovirus%Mice%Arteriosclerosis%Fluvastatin
目的 探讨巨细胞病毒(Cytomegalovirus)与动脉粥样硬化(Atherosclerosis,AS)形成的相关性及氟伐他汀对其的影响.方法 以载脂蛋白E基因缺陷(Apolipoprotein-E Knockout,apoE-/-)小鼠为研究对象,给予低剂量小鼠巨细胞病毒(Murine Cytomegalovirus,MCMV),观察动脉粥样硬化病变的变化.并在氟伐他汀的干预下,观察病毒感染对AS的影响,以探讨MCMV在动脉粥样硬化形成及发展过程中所起的作用.结果 研究显示在慢性潜伏感染阶段,MCMV感染明显加重apoE-/-小鼠动脉粥样硬化病变面积;小鼠动脉壁中没有MCMV mRNA的表达;血浆MCMV抗体水平、唾液腺MCMV DNA含量和动脉粥样硬化病变程度没有相关性.氟伐他汀干预后,MCMV感染组与未感染组在AS病变的面积、数目、内膜/中膜比值方面的显著性差异消失.结论 在慢性潜伏感染阶段,MCMV感染可以明显加重apoE-/-小鼠主动脉AS病变,但在血管壁局部并无MCMV活动性感染的证据.氟伐他汀可以改善MCMV感染后apoE-/-小鼠的AS病变进程.但这种作用并不是通过减少病毒量来实现的.
目的 探討巨細胞病毒(Cytomegalovirus)與動脈粥樣硬化(Atherosclerosis,AS)形成的相關性及氟伐他汀對其的影響.方法 以載脂蛋白E基因缺陷(Apolipoprotein-E Knockout,apoE-/-)小鼠為研究對象,給予低劑量小鼠巨細胞病毒(Murine Cytomegalovirus,MCMV),觀察動脈粥樣硬化病變的變化.併在氟伐他汀的榦預下,觀察病毒感染對AS的影響,以探討MCMV在動脈粥樣硬化形成及髮展過程中所起的作用.結果 研究顯示在慢性潛伏感染階段,MCMV感染明顯加重apoE-/-小鼠動脈粥樣硬化病變麵積;小鼠動脈壁中沒有MCMV mRNA的錶達;血漿MCMV抗體水平、唾液腺MCMV DNA含量和動脈粥樣硬化病變程度沒有相關性.氟伐他汀榦預後,MCMV感染組與未感染組在AS病變的麵積、數目、內膜/中膜比值方麵的顯著性差異消失.結論 在慢性潛伏感染階段,MCMV感染可以明顯加重apoE-/-小鼠主動脈AS病變,但在血管壁跼部併無MCMV活動性感染的證據.氟伐他汀可以改善MCMV感染後apoE-/-小鼠的AS病變進程.但這種作用併不是通過減少病毒量來實現的.
목적 탐토거세포병독(Cytomegalovirus)여동맥죽양경화(Atherosclerosis,AS)형성적상관성급불벌타정대기적영향.방법 이재지단백E기인결함(Apolipoprotein-E Knockout,apoE-/-)소서위연구대상,급여저제량소서거세포병독(Murine Cytomegalovirus,MCMV),관찰동맥죽양경화병변적변화.병재불벌타정적간예하,관찰병독감염대AS적영향,이탐토MCMV재동맥죽양경화형성급발전과정중소기적작용.결과 연구현시재만성잠복감염계단,MCMV감염명현가중apoE-/-소서동맥죽양경화병변면적;소서동맥벽중몰유MCMV mRNA적표체;혈장MCMV항체수평、타액선MCMV DNA함량화동맥죽양경화병변정도몰유상관성.불벌타정간예후,MCMV감염조여미감염조재AS병변적면적、수목、내막/중막비치방면적현저성차이소실.결론 재만성잠복감염계단,MCMV감염가이명현가중apoE-/-소서주동맥AS병변,단재혈관벽국부병무MCMV활동성감염적증거.불벌타정가이개선MCMV감염후apoE-/-소서적AS병변진정.단저충작용병불시통과감소병독량래실현적.
Objective The goal of this study was to investigate whether murine cytomegalovirus (MCMV) is able to exacerbate the atherosclerotic process in apolipoprotein E knockout (apoE-/-) mice,and the effect of fluvastatin on the atherogenesis. Methods The apoE -/- mice kept on a west diet were given low dosage of MCMV. At 14,18 and 24 weeks post infection, AS lesion were measured on aorta. The fluvastatin was administered,and AS lesion were measured accordingly above. Results We observed that in the chronic phase of the infection, AS lesion area was significantly increased. MCMV gB mRNA was not amplified by real-time PCR from the arterial wall. The IgG antibody level of MCMV in blood plasma and the content of virus DNA in salivary gland were not correlated with AS lesions. After the administration of fluvastatin, there was no significant difference of AS lesions between MCMV infected group and mockinfected group. Conclusion MCMV may aggravate the AS lesion in apoE -/- mice in the chronic phase of infection, and promote more severe type of AS lesions. But it might not be the direct effects of mechanism of MCMV on the local lesion of AS. Fluvastatin could meliorate the progression of AS after MCMV infection,but this was not accomplished by decreasing MCMV duplication.