Effects Of Pparγ Agonists On Atherosclerosis Lesion And The Chemotactic Factor Ccl21 And Its Receptor Ccr7 In High Cholesterol-diet In Apolipoprotein E Knock-out Mice

Objective: To investigate the potential effects of PPARγagonist Rosiglitazone on the atherosclerosis lesion and chemokine ligand CCL21 and chemokine receptor CCR7 in high cholesterol-diet (HCD) apolipoprotein E knock-out (ApoE K O) mice.Methods: 40 ApoE KO mice were randomly divided into 5 groups, given normal diet(ND) or HCD and randomized to no treatment or rosiglitazone 5mg.kg-1.d-1 or rosiglitazone 10mg.kg-1.d-1 or rosiglitazone 20mg.kg-1.d-1 for 12weeks groop. The plasma levels of chemokine ligand CCL21 were measured with ELISA method, and its chemokine recptor CCR7 were measured by real-time reverse transcription Fluourescent Quantitative polymerase chain reaction (RT- PCR ), The plasma total cholesterol and triglyceride and low density lipoprotein and high-sensitivity C-reactive protein (hs-CRP) concentration were measured by autoanalyzer, Atherosclerotic lesion area in aortic root was evaluated by HE staining with Densitograph Imaging Software.Results :The ApoE KO mice with HCD was associated with a marked increase in plasma lipid levels ,hs-CRP,atherosclerotic lesion area, as well as the expressions of chemokine ligand CCL21. These changes were suppressed in mice treated with Rosiglitazone for 12 weeks concomitant with HCD administration .But the changes of CCR7 were significantly promoted in mice treated with Rosiglitazone .Conclusion: Rosiglitazone could attenuate atherosclerosis, and this effect was in part related to inhibition expressions of chemokine ligand CCL21and to promote expressions of chemokine recptor CCR7.