title: [Impact of exogenous fibroblast growth factor 21 on atherosclerosis in apolipoprotein E deficient mice].
abstract: OBJECTIVE
  To explore the effects and related mechanisms of exogenous fibroblast growth factor (FGF) 21 on atherosclerosis in apolipoprotein E deficient (apoE-/-) mice.
  
  
  METHODS
  Male 17-week-old C57BL/6J mice and apoE-/- mice were randomly divided into three groups (n = 12 each): blank control group (C vehicle), atherosclerosis group without FGF21 (apoE-/- vehicle) and apoE-/- plus FGF21 (100 µg × kg⁻¹ × d⁻¹ subcutaneously treatment) . All mice were fed with high-fat diet for 4 weeks. After 4 weeks treatments, atherosclerotic lesions in aortic arch and inner diameter of abdominal aorta were measured by ultrasonography. Plasma lipid profiles, CRP and TNFα were measured. The whole aorta and aortic root were prepared for HE and oil red O staining to analyze lesion areas.
  
  
  RESULTS
  There was no evident plaque in C vehicle group. TC/HDL-C, LDL-C/HDL-C, non-HDL-C, expression of CRP and TNFα were significantly higher in apoE-/- vehicle group than in C vehicle group (all P < 0.05). IMT of aorta [(156.4 ± 17.6)µm vs. (57.8 ± 7.4)µm] were significantly higher in apoE-/- vehicle group than in C vehicle group (all P < 0.05). While FGF21 significantly reduced the lesion area in aorta arch [(1.42 ± 0.16) mm² vs. (2.30 ± 0.10) mm², P < 0.05] and the inner diameter of abdominal aorta [(0.97 ± 0.03) mm vs. (0.75 ± 0.18) mm, P < 0.05] compared to apoE-/- vehicle group. Similarly, TC/HDL-C(5.11 ± 0.70), LDL-C/HDL-C(3.90 ± 0.76), non-HDL-C[(6.33 ± 1.22)mmol/L], plasma CRP[(4.20 ± 1.03)mmol/L] and plasma TNFα[(1.29 ± 0.47)mmol/L] were also reduced by FGF21( all P < 0.05 vs. apoE-/- vehicle). Moreover, FGF21 decreased the IMT[(107.2 ± 33.5)µm vs. (156.4 ± 17.6)µm], lesion area of aorta [(14.26 ± 3.5)%] vs. [(23.06 ± 4.16)%] and plaque size of aorta root [(21.75 ± 7.14)% vs. (38.03 ± 5.76)%] (all P < 0.05 vs. apoE-/- vehicle).
  
  
  CONCLUSIONS
  FGF21 can protect apoE-/- mice from atherosclerosis by modifying lipid profiles and downregulating CRP and TNFα expressions.
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Xi
authors.initials: X
authors.lastname: Wu
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Lü
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Kun
authors.initials: K
authors.lastname: Fu
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Shaoping
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Donghui
authors.initials: D
authors.lastname: Zhao
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Hongyu
authors.initials: H
authors.lastname: Peng
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Fan
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Lü
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
authors.forename: Mankun
authors.initials: M
authors.lastname: Xin
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China. Email: liujinghua@vip.sina.com.
authors.forename: Jinghua
authors.initials: J
authors.lastname: Liu
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics; D050197:Atherosclerosis / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D002097:C-Reactive Protein / Q000378:metabolism; D004195:Disease Models, Animal; D005346:Fibroblast Growth Factors / Q000494:pharmacology*; D008055:Lipids / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D058226:Plaque, Atherosclerotic / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D001057:Apolipoproteins E; D008055:Lipids; D014409:Tumor Necrosis Factor-alpha; C414620:fibroblast growth factor 21; D005346:Fibroblast Growth Factors; D002097:C-Reactive Protein