Yi Li, Wang Jia-Wei, Zhao Ri-Guang, Tuo Hou-Zhen, Feng Zi-Jing, Wang De-Xin
Department of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2010 Dec;24(6):433-5.
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.
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.
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 mock-infected group.
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.
本研究旨在调查鼠巨细胞病毒(MCMV)是否能够加剧载脂蛋白E基因敲除(apoE-/-)小鼠的动脉粥样硬化进程,以及氟伐他汀对动脉粥样硬化发生的影响。
给予食用西方饮食的apoE-/-小鼠低剂量的MCMV。在感染后14、18和24周,测量主动脉上的动脉粥样硬化(AS)病变。给予氟伐他汀,并相应地测量上述AS病变。
我们观察到在感染的慢性期,AS病变面积显著增加。实时PCR未从动脉壁扩增出MCMV gB mRNA。血浆中MCMV的IgG抗体水平和唾液腺中病毒DNA的含量与AS病变无关。给予氟伐他汀后,MCMV感染组和假感染组之间的AS病变无显著差异。
MCMV可能在感染的慢性期加重apoE-/-小鼠的AS病变,并促进更严重类型的AS病变。但这可能不是MCMV对AS局部病变的直接作用机制。氟伐他汀可改善MCMV感染后AS的进展,但这并非通过减少MCMV复制来实现。