TAILIEUCHUNG - Báo cáo y học: "Nociceptive tolerance is improved by bradykinin receptor B1 antagonism and joint morphology is protected by both endothelin type A and bradykinin receptor B1 antagonism in a surgical model of osteoarthritis"

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: Nociceptive tolerance is improved by bradykinin receptor B1 antagonism and joint morphology is protected by both endothelin type A and bradykinin receptor B1 antagonism in a surgical model of osteoarthritis. | Kaufman et al. Arthritis Research Therapy 2011 13 R76 http content 13 3 R76 RESEARCH ARTICLE Open Access Nociceptive tolerance is improved by bradykinin receptor B1 antagonism and joint morphology is protected by both endothelin type A and bradykinin receptor B1 antagonism in a surgical model of osteoarthritis Gabriel N Kaufman1 Charlotte Zaouter1 Barthélémy Valteau2 Pierre Sirois3 and Florina Moldovan1 4 Abstract Introduction Endothelin-1 a vasoconstrictor peptide influences cartilage metabolism mainly via endothelin receptor type A ETA . Along with the inflammatory nonapeptide vasodilator bradykinin BK which acts via bradykinin receptor B1 BKB1 in chronic inflammatory conditions these vasoactive factors potentiate joint pain and inflammation. We describe a preclinical study of the efficacy of treatment of surgically induced osteoarthritis with ETA and or BKB1 specific peptide antagonists. We hypothesize that antagonism of both receptors will diminish osteoarthritis progress and articular nociception in a synergistic manner. Methods Osteoarthritis was surgically induced in male rats by transection of the right anterior cruciate ligament. Animals were subsequently treated with weekly intra-articular injections of specific peptide antagonists of ETA and or BKB1. Hind limb nociception was measured by static weight bearing biweekly for two months post-operatively. Post-mortem right knee joints were analyzed radiologically by X-ray and magnetic resonance and histologically by the OARSI histopathology assessment system. Results Single local BKB1 antagonist treatment diminished overall hind limb nociception and accelerated post-operative recovery after disease induction. Both ETA and or BKB1 antagonist treatments protected joint radiomorphology and histomorphology. Dual ETA BKB1 antagonism was slightly more protective as measured by radiology and histology. Conclusions BKB1 antagonism improves nociceptive tolerance and both ETA and or BKB1 .

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