Elvenes Jan, Andjelkov Nenad, Figenschau Yngve, Seternes Tore, Bjørkøy Geir, Johansen Oddmund
Department of Orthopaedic Surgery, University Hospital of Northern-Norway, 9038 Tromsø, Norway.
Biochem Biophys Res Commun. 2003 Nov 7;311(1):202-7. doi: 10.1016/j.bbrc.2003.09.191.
There is evidence of effects of morphine on cell proliferation and intraarticular morphine produces analgesia and has an anti-inflammatory effect in chronic arthritis. The effects of opioids are mediated through the G-protein-coupled receptors affecting the cAMP pathway. We demonstrated that human osteoarthritic cartilage and cultured chondrocytes possess the mu-opioid receptor. The presence of the receptor was shown by immunodetection, polymerase chain reaction, and Western blotting. Stimulation of chondrocytes with beta-endorphin resulted in decreased phosphorylation of the transcription factor cAMP responsive element binding protein (CREB). The effect was reversed by naltrexone. The obtained results indicate that in human articular chondrocytes opioids affect, via the mu-opioid receptor, the transcription factor CREB which in turn can cause subsequent changes in gene expression.
有证据表明吗啡对细胞增殖有影响，关节内注射吗啡可产生镇痛作用，并对慢性关节炎有抗炎作用。阿片类药物的作用是通过影响环磷酸腺苷（cAMP）途径的G蛋白偶联受体介导的。我们证明人类骨关节炎软骨和培养的软骨细胞具有μ-阿片受体。通过免疫检测、聚合酶链反应和蛋白质印迹法显示了该受体的存在。用β-内啡肽刺激软骨细胞导致转录因子环磷酸腺苷反应元件结合蛋白（CREB）的磷酸化减少。纳曲酮可逆转该效应。所得结果表明，在人类关节软骨细胞中，阿片类药物通过μ-阿片受体影响转录因子CREB，进而可能导致基因表达的后续变化。
