title: [Protective effect of acupuncture on heart in mice with hyperlipemia and its mechanism].
abstract: OBJECTIVE
  To observe the inhibiting effect of acupuncture on blood lipid, myocardial hypertrophy and fibrosis in mice with hyperlipemia, and explore its possible action mechanism.
  
  
  METHODS
  Ten inbred mice (C57) were applied. Forty ApoE(-/-) mice who removed gene of apolipoprotein E were randomly divided into a control group, a non-acupoint group, an acupoint group and a medication group. The points 0. 5 cm and 1 cm next to the end of mice tail were respectively punctured in the non-acupoint group; "Neiguan" (PC 6) and "Fenglong" (ST 40) were punctured in the acupoint group; intragastric administration of simvastatin was applied in the medication group. After 8 weeks of treatment, the changes of total cholesterol (TC) and ratio of heart to body mass in each group were measured; changes of cardiac muscle fiber and ventricular wall thickness were observed; enzyme linked immunosorbent assay (ELISA) was used to test the level of angiotensin II (Ang I ) in plasma, and western blotting method was used to test protein content of angiotensin II type 1 receptor (AT1R) and endothelin-1 type A receptor (ETAR) in the heart.
  
  
  RESULTS
  After 8 weeks of intervention, compared with the control group, rising range of blood lipid was obviously decreased (P<0.01) in the acupoint group and medication group, ratio of P<0.01), myocardial heart to body mass was decreased (P<0.05), thickness of ventricular wall was reduced (P fibrosis was relieved, levels of Ang II and ET-1 in plasma were decreased (P<0. 05), content of NO was increased (P<0. 05), and protein content of AT1R and ETAR was decreased in the heart (P<0. 05).
  
  
  CONCLUSIONS
  40) could inhibit the rising of blood lipid in ApoE(-/-) mice, lower the levels of Ang II and ET-1 in peripheral blood, increase the content of NO and inhibit the expression of AT1R and ETAR in heart tissue, which could relieve myocardial hypertrophy and fibrosis to play a protective role on heart.
authors.forename: Hong-Bo
authors.initials: HB
authors.lastname: Shen
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.forename: Jia
authors.initials: J
authors.lastname: Guo
authors.forename: Xiao-Lan
authors.initials: XL
authors.lastname: Ji
authors.forename: Bo
authors.initials: B
authors.lastname: Peng
authors.forename: Fu-Yun
authors.initials: FY
authors.lastname: Li
authors.forename: Cheng
authors.initials: C
authors.lastname: Liu
authors.forename: Ze-jun
authors.initials: ZJ
authors.lastname: Huo
mesh_terms: D015669:Acupuncture Points; D015670:Acupuncture Therapy; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D006331:Heart Diseases / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism
chemical_list: D000804:Angiotensin II