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Inhibitory Effect of Electroacupuncture on Murine Collagen Arthritis and its Possible Mechanisms

  • Fang, Jian-Qiao (Department of Physiology, School of Medicine, Showa University) ;
  • Aoki, Eri (Department of Physiology, School of Medicine, Showa University) ;
  • Yu, Ying (Department of Physiology, School of Medicine, Showa University) ;
  • Sohma, Toshimitsu (Department of Physiology, School of Medicine, Showa University) ;
  • Kasahara, Takako (Department of Physiology, School of Medicine, Showa University) ;
  • Hisamitsu, Tadashi (Department of Physiology, School of Medicine, Showa University)
  • Published : 2001.02.28

Abstract

The influence of electroacupuncture (EA), a traditional Chinese medical treatment, on type Ⅱ collagen-induced arthritis (CIA) was examined in DBA/1J mice in vivo. Mice were immunized intradermally twice at the 3-week interval with bovine type Ⅱ collagen(C Ⅱ). EA stimulation, begun on the 21 simultaneously with the second immunization, was applied at the acupoint equivalent to GV4 three times a week for 3 weeks. The results showed that EA delayed the onset, attenuated the severity of arthritis, and reduced the anti-collagen antibody level. Furthermore, we investigated the impact of EA on the productions of endogenous $interleukin-1{\Beta}$ (IL-1 beta) and prostaglandin E2 (PGE2), and the levels of IL-1 beta mRNA in splenocytes and synovial tissues from C Ⅱ immunized mice on the 45 and cyclooxygenase-2 (COX-2) mRNA in lipopolysaccharide (LPS)-stimulated macrophages of normal mice by using reverse transcriptase-polymerase chain reaction (RT-PCR). EA stimulation significant inhibited the concentrations of splenic endogenous IL-1 beta and serum PGE2. The expression of IL-1 beta mRNA in spleen cells was obviously down-regulated and that in synovial tissues was modestly affected by EA. COX-2 mRNA was highly expressed in cultured peritoneal macrophages when stimulated with LPS. Previous treatment with EA also reduced LPS-stimulated induction of COX-2 mRNA. These data suggest that EA has an inhibitory effect on murine CIA, and the partial mechanism of its therapeutic result may be attributed to inhibiting the productions of IL-1 beta and PGE2 by suppression the IL-1 beta and COX-2 gene activations.

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