Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài:Differential effects of locally and systemically administered soluble glycoprotein 130 on pain and inflammation in experimental arthritis. | Boettger et al. Arthritis Research Therapy 2010 12 R140 http content 12 4 R140 RESEARCH ARTICLE Open Access Differential effects of locally and systemically administered soluble glycoprotein 130 on pain and inflammation in experimental arthritis Michael K Boettger1 Johannes Leuchtweis1 Diana Kummel1 Mieczyslaw Gajda2 Rolf Brauer2 Hans-Georg Schaible1 Abstract Introduction Interleukin-6 IL-6 is a key player in systemic arthritis involved in inflammation and joint destruction. IL-6 signalling has also been revealed in nerve cells. Recently IL-6 and in particular IL-6 together with its soluble IL-6 receptor sIL-6R were shown to induce a long-lasting robust sensitization of joint nociceptors for mechanical stimuli which was difficult to reverse suggesting that IL-6 signalling plays a significant role in the generation and maintenance of arthritic pain. Here we tested in a preclinical model of arthritis antigen-induced arthritis AIA in the rat whether systemic or local neutralization of IL-6 sIL-6R complexes with soluble glycoprotein 130 sgp130 alters arthritic pain and how sgp130 influences the inflammatory process in AIA. Methods Rats with AIA were either treated with sgp130 or saline intra-peritoneally or intra-articularly each group n 9 . Then pain-related and locomotor behaviour as well as joint swelling were measured during an observation period of 21 days followed by histopathological end-point analysis for inflammatory and destructive changes. Results A single intra-articular application of sgp130 at the time of AIA induction barely reduced the development of AIA but significantly attenuated pain-related behaviour that is primary mechanical hyperalgesia in the acute phase of AIA. By contrast repeated systemic application of sgp130 after onset of AIA only slightly attenuated pain at a late stage of AIA. None of the treatments reduced secondary hyperalgesia. Furthermore in the present study joint destruction at 21 days was significantly .
