Establishment of a Wuzhishan minipig model of atherosclerosis induced by high fat/cholesterol diet and regulation of Lp-PLA2 expression
10.3969/j.issn.1005-4847.2017.02.015
- VernacularTitle:高脂诱导五指山小型猪动脉粥样硬化模型的建立及Lp-PLA2的表达调控
- Author:
Jing WANG
;
Yongming PAN
;
Xiaoping XU
;
Yueqin CAI
;
Fangming CHEN
;
Zhaowei CAI
;
Minli CHEN
- Keywords:
Wuzhishan minipig;
Atherosclerosis;
Lipoprotein associated phospholipase A2;
Inflammation
- From:
Acta Laboratorium Animalis Scientia Sinica
2017;25(2):194-200
- CountryChina
- Language:Chinese
-
Abstract:
Objective To establish a Wuzhishan minipig model of atherosclerosis(AS) induced by high fat/cholesterol diet,and observe the changes of expression of lipoprotein associated phospholipase A2(Lp-PLA2) in plasma and plaques.Methods 10 Wuzhishan minipigs were randomly divided into 2 groups:The normal control(Ctr,n=4) group was fed with normal diet,and AS model(n=6) group fed with high fat/cholesterol diet for 24 weeks.After the modeling for 24 weeks,the changes of total cholesterol(TC),low density lipoprotein(LDL-C),high density lipoprotein(HDL-C),triglyceride(TG),C-reactive protein(CRP),Lp-PLA2 activity and composition were detected.The changes of vascular lipid deposition and plaques were assessed by pathology using oil red O staining and HE staining,respectively,and immunohistochemical staining for IL-6 protein expression.Moreover,the expression of Lp-PLA2 mRNA determined by RT-PCR and protein by Western blot were observed in the abdominal aortic tissues.Results Compared with the control group,the body weight,body mass index(BMI),TC,LDL-C,HDL-C,CRP,Lp-PLA2 activity and composition and aortic lipid deposition were significantly increased,and AS plaque formation was observed in the AS model group(P<0.05,P<0.01).The expression of Lp-PLA2mRNA and protein and IL-6 protein in abdominal aortic tissues were also significantly increased(P<0.05).Conclusions Long-term high fat/cholesterol diet feeding for 24 weeks can induce atherosclerosis in Wuzhishan minipigs,and Lp-PLA2 plays a key role in the vascular inflammation and plaque formation.
