title: [Anti-atherosclerotic Effects of Bear Bile Powder in Shexiang Tongxin Dripping Pill: a Mechanism Study].
abstract: OBJECTIVE : To study the anti-atherosclerotic mechanism of bear bile powder (BBP) in Shexiang Tongxin Dripping Pill (STDP) , and to provide scientific evidence for treating atherosclerosis (AS) by its therapeutic characteristics of cool resuscitation.
  
  
  METHODS
  AS model was duplicated using ApoE-/- gene knocked mice fed with high-fat diet. Thirty ApoE-/- deficient male mice were divided into four groups according to body weight using random digit table, i.e., the model group (A, n =9), the STDP group (B, n=E7), the STDP without BBP group (C, n =7), and the BBP group (D, n =9). Besides, another 9 C57BL/6J male mice of the same age were recruited as a normal control group (E). All mice in Group B, C, and D were respectively administered with corresponding drugs (30, 30, and 0. 33 mg/kg) by gastrogavage. Equal volume of normal saline was administered to mice in Group A and E. All medication lasted for 8 successive weeks. Serum levels of inflammatory cytokines such as interleukin 2 (IL-2), interleukin 6 (IL-6), tumor necrosis factor a (TNF-α), interferon y (IFNγ), and oxidized low-density lipoprotein (ox-LDL) were measured by ELISA. Serum levels of malondialdehyde (MDA), activities of glutathione (GSH) and superoxide dismutase (SOD) were determined using biochemical assay. Contents of reactive oxygen species (ROS) in the aortic root was detected by dihydroethidum (DHE) fluorescent probe. Expression levels of microRNAs (such as miR-20, miR-21, miR-126, and miR-155) were detected by real-time PCR.
  
  
  RESULTS
  The fluorescence intensity of the aorta was obviously enhanced in Group A. But it was obviously attenuated in Group B, C, and D, and the attenuation was the most in Group B. Compared with Group E, serum levels of IL-2, IL-6, TNF-α, IFN-γ, oxLDL, and MDA all increased (P <0. 01), GSH contents and SOD activities decreased (P <0. 01), expression levels of miR-126, miR-21, and miR-155 in aorta increased (P <0. 01), and the expression level of miR-20 decreased in Group A (P<0. 01). Compared with Group A, serum levels of IL-2, IL-6, TNF-α, IFN-γ, oxLDL, and MDA were all down-regulated (P <0. 01), GSH contents and SOD activities were up-regulated (P <0. 01), expression levels of miR-126, miR-21, and miR-155 in aorta were down-regulated in Group B, C, and D (P <0. 01). The expression level of miR20 was up-regulated in Group B and D (P <0. 01). Compared with Group B, serum levels of IL-2, IL-6, TNF-α, IFN-γ increased (P <0.01); GSH contents and SOD activities decreased, levels of MDA and oxLDL increased (P <0. 01) in Group C and D. Expression levels of miR-20 and miR-155 were down-regulated in Group C and D (P <0. 01).
  
  
  CONCLUSIONS
  STDP played roles in significantly regulating inflammatory factors and oxidative stress factors. Its mechanism might be possibly associated with regulating expressions of miR-126, miR-21, miR-155, and miR-20 in aorta. BBP played significant roles in STDP.
authors.forename: Min-qi
authors.initials: MQ
authors.lastname: Xiong
authors.forename: Cheng-lin
authors.initials: CL
authors.lastname: Jia
authors.forename: Jing-gang
authors.initials: JG
authors.lastname: Cui
authors.forename: Bing-bing
authors.initials: BB
authors.lastname: Ming
authors.forename: Yu-ling
authors.initials: YL
authors.lastname: Zhu
authors.forename: Wen-jian
authors.initials: WJ
authors.lastname: Wang
authors.forename: Yu
authors.initials: Y
authors.lastname: Chen
authors.forename: Teng
authors.initials: T
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001011:Aorta; D001057:Apolipoproteins E / Q000378:metabolism; D050197:Atherosclerosis; D001646:Bile; D016207:Cytokines; D059305:Diet, High-Fat; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress; D058226:Plaque, Atherosclerotic / Q000188:drug therapy*; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D001503:Ursidae
chemical_list: D001057:Apolipoproteins E; D016207:Cytokines; D004365:Drugs, Chinese Herbal; C508600:IL6 protein, human; D015850:Interleukin-6; D008077:Lipoproteins, LDL; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; C099252:oxidized low density lipoprotein; D008315:Malondialdehyde; D013482:Superoxide Dismutase