title: [Effects of dioscornin tablet containing serum on NF-kappaB p65, STAT3, and VEGF mRNA expressions in rats' synovial cell strain RSC-364 induced by IL-17 and TNF-alpha].
abstract: OBJECTIVE
  To observe the effects of Dioscornin Tablet (DT) containing serum on nuclear factor of kappa B (NF-kappaB) p65, signal transducer and activator of transcription 3 (STAT3), and vascular endothelial growth factor (VEGF) mRNA expressions in rats' synovial cell strain 364 (RSC-364) induced by interleukin-17 (IL-17) and tumor necrosis factor-alpha (TNF-alpha), and to investigate the underlying mechanisms for DT to inhibit angiogenesis of rheumatoid arthritis (RA).
  
  
  METHODS
  In this experiment, the vehicle control group, the cell model group, the DT containing serum group, and the positive control group (Tripterygium containing serum) were set up. The DT containing serum and the Tripterygium containing serum were prepared. The RA cell model was established by IL-17 combined TNF-alpha induced injury in RSC-364. The RA cells were intervened by DT containing serum and Tripterygium containing serum respectively. The DNA binding activity of NF-kappaB p65 was detected using TransAM NF-kappaB p65. The expression of STAT3 was observed using Western blot. The VEGF mRNA expressions were detected by real-time quantitative PCR.
  
  
  RESULTS
  Compared with the vehicle control group, the NF-kappaB p65 activity, the expressions of STAT3 and VEGF mRNA increased significantly in RSC-364 induced by IL-17 +TNF-alpha (P < 0.01, P < 0.05). Compared with the model group, the NF-kappaB p65 activity, the expressions of STAT3 and VEGF mRNA decreased significantly in the DT containing serum group and the positive control group (P < 0.01, P < 0.05). There was no statistical difference between the two groups (P > 0.05).
  
  
  CONCLUSIONS
  DT inhibited the VEGF mRNA expression through inhibiting the NF-kappaB p65 activity and the STAT3 protein expression in the Janus kinase (JAK)-signal transducer and activating transcription factor pathway, thus inhibiting the angiogenesis of RA.
authors: Department of Pathogen Biology, Chengde Medical College, Hebei 067000, China.
authors: Ya-Chun
authors: YC
authors: Guo
authors: Ya-Xian
authors: YX
authors: Gao
authors: Hong-Ru
authors: HR
authors: Song
mesh_terms: D000818:Animals; D001172:Arthritis, Rheumatoid / Q000473:pathology; D002478:Cells, Cultured; D004144:Diosgenin / Q000031:analogs & derivatives* / Q000494:pharmacology; D020381:Interleukin-17 / Q000009:adverse effects; D008297:Male; D009389:Neovascularization, Pathologic / Q000473:pathology; D012333:RNA, Messenger / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D050796:STAT3 Transcription Factor / Q000378:metabolism; D044967:Serum; D015398:Signal Transduction; D013583:Synovial Membrane / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000009:adverse effects; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D020381:Interleukin-17; D012333:RNA, Messenger; C498145:Rela protein, rat; D050796:STAT3 Transcription Factor; C494088:Stat3 protein, rat; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; C019357:dioscin; D004144:Diosgenin