Publisher： Spandidos Publications
E-ISSN： 1791-3004|12|4|6145-6151
ISSN： 1791-2997
Source： Molecular Medicine Reports, Vol.12, Iss.4, 2015-01, pp. : 6145-6151
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Abstract
Atherosclerosis is a chronic inflammatory response of the arterial wall to proatherosclerotic factors. As an inflammatory marker, fibrinogen directly participates in the pathogenesis of atherosclerosis. Our previous study demonstrated that fibrinogen and fibrin degradation products (FDP) produce a proinflammatory effect on vascular smooth muscle cells (VSMCs) through inducing the production of interleukin6 (IL6), tumor necrosis factorα (TNFα) and inducible nitric oxide synthase (iNOS). In the present study, the effects of pravastatin on fibrinogen and FDPinduced expression of IL6, TNFα and iNOS were observed in VSMCs. The results showed that pravastatin dosedependently inhibited fibrinogen and FDPstimulated expression of IL6, TNFα and iNOS in VSMCs at the mRNA and protein level. The maximal inhibition of protein expression of IL6, TNFα and iNOS was 46.9, 42.7 and 49.2% in fibrinogenstimulated VSMCs, and 50.2, 49.8 and 53.6% in FDPstimulated VSMCs, respectively. This suggests that pravastatin has the ability to relieve vascular inflammation via inhibiting the generation of IL6, TNFα and iNOS. The results of the present study may aid in further explaining the beneficial effects of pravastatin on atherosclerosis and related cardiovascular diseases. In addition, they suggest that application of pravastatin may be beneficial for prevention of atherosclerosis formation in hyperfibrinogenemia.
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