title: [The protective mechanism study of fengshiqing recipe against bone destruction in CIA rats].
abstract: OBJECTIVE
  To explore the protective mechanism of Fengshiqing Recipe (FR) against bone destruction in collagen-induced arthritis (CIA) rats.
  
  
  METHODS
  Rats were divided into four groups in the experiment,i.e., the blank control group, the model group, the MTX group (MTX, 1 mg/1 000 g), and the FR group (24 g crude FR/kg). The CIA model was prepared except the blank control group. Medication was started in the MTX group and the FR group from the 14th day after modeling to the 56th day. The toe volume was measured on every Tuesday and Friday. Expression levels of serum IL-17, RANKL, MIP-1alpha were detected after 3-and 6-week intervention. The bone scintigraphy with nuclide (SPECT), bone mineral density (BMD), and the pathological section were observed to assess the intervention of drugs of heat clearing blood activating actions in the bone destruction of CIA rats.
  
  
  RESULTS
  From the 10th day of modeling, the volume of both toes started to swell and reached the peak at about 21 days. It was obviously shrunk at about 30 days. Of them, the swelling degree was milder in the MTX group and the FR group than in the model group. Compared with the model group at the same phase, the levels of IL-17 and RANKL decreased in the MTX group after 3 weeks of intervention (P < 0.01, P < 0.05). The IL-17 level decreased in the FR group after three weeks of intervention (P < 0.05). The RANKL level decreased in the MTX group and the FR group after 6 weeks of intervention (P < 0.01, P < 0.05). Compared with the model group and the MTX group, the overall BMD and ankle BMD increased in the FR group after 6 weeks of intervention (P < 0.01, P < 0.05). The ankle ROI/mandible and the toe ROI/mandible were elevated in the FR group after 3 weeks of intervention (P < 0.05). Pathological results suggested that the joint lacunae was significantly widened, the hyperplasia of the synovial tissue was so severe, and the bone tissue was destroyed in the model group. Compared with the model group, the aforesaid conditions were significantly improved in the MTX group and the FR group. The cartilage structure was complete.
  
  
  CONCLUSIONS
  QR could inhibit decreased BMD, prevent bone destruction, which might be achieved by down-regulating expression levels of IL-17, RANKL, and MIP-1alpha through the osteo immunological Th/RANKL system,inhibiting maturation and differentiation of osteoclasts, thereby, inhibiting bone destruction.
authors: Department of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Quan
authors: Q
authors: Jiang
authors: Pharmacy College, Beijing University of Chinese Medicine, Beijing 100102, China.
authors: De-Ping
authors: DP
authors: Li
authors: Department of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Wei
authors: W
authors: Cao
authors: Department of Immunology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Guang-Jun
authors: GJ
authors: Wu
authors: Department of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Xiao-Po
authors: XP
authors: Tant
authors: Pharmacy College, Beijing University of Chinese Medicine, Beijing 100102, China.
authors: Yun
authors: Y
authors: Lei
authors: Department of Nuclear Medicine, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Jia-Xiu
authors: JX
authors: Li
authors: Department of Endocrinology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Hao-Chen
authors: HC
authors: Kang
authors: Department of Nuclear Medicine, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Bo
authors: B
authors: Gao
authors: Department of Nuclear Medicine, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Guang
authors: G
authors: Lei
authors: Department of Nuclear Medicine, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Chun-Hong
authors: CH
authors: Zhai
authors: Pharmacy College, Beijing University of Chinese Medicine, Beijing 100102, China.
authors: Hua-Qiang
authors: HQ
authors: Zhai
authors: Department of Immunology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Zhen-Yu
authors: ZY
authors: Wu
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000188:drug therapy* / Q000378:metabolism*; D015519:Bone Density; D001842:Bone and Bones / Q000187:drug effects / Q000473:pathology*; D054405:Chemokine CCL3 / Q000378:metabolism; D004365:Drugs, Chinese Herbal / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D020381:Interleukin-17 / Q000378:metabolism; D053245:RANK Ligand / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D054405:Chemokine CCL3; D004365:Drugs, Chinese Herbal; C515934:Il17a protein, rat; D020381:Interleukin-17; D053245:RANK Ligand