Fluvastatin's effect on atherogenesis in apolipoprotein-E knockout mice infected by cytomegalovirus.
- Author:
Li YI
1
;
Jia-Wei WANG
;
Ri-Guang ZHAO
;
Hou-Zhen TUO
;
Zi-Jing FENG
;
De-Xin WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Aorta; drug effects; Apolipoproteins E; deficiency; genetics; Atherosclerosis; blood; drug therapy; genetics; virology; Fatty Acids, Monounsaturated; pharmacology; Herpesviridae Infections; blood; drug therapy; virology; Immunoglobulin G; blood; Indoles; pharmacology; Male; Mice; Mice, Knockout; Muromegalovirus; genetics
- From: Chinese Journal of Experimental and Clinical Virology 2010;24(6):433-435
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEThe 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.
METHODSThe 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.
RESULTSWe 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.
CONCLUSIONMCMV 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.
