微分的监管职责的垂体腺苷酸cyclase-activating多肽serum-transfer关节炎模型。

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Botz B, Bolcskei K, Kereskai L, Kovacs M, Nemeth T, Szigeti K,霍我装置建立D, Kovacs N,桥本H, Reglodi D, Szolcsanyi J,品特E, Mocsai, Helyes Z

微分的监管职责的垂体腺苷酸cyclase-activating多肽serum-transfer关节炎模型。

关节炎Rheumatol。2014年10月,66 (10):2739 - 50。doi: 10.1002 / art.38772。

PubMed ID

25048575 (在PubMed

]

文摘

摘要目的:垂体腺苷酸cyclase-activating多肽(PACAP)表达capsaicin-sensitive感觉神经元在炎症和免疫细胞有不同的功能和痛苦的过程。本研究是探讨PACAP参与风湿性关节炎的小鼠模型。方法:关节炎在PACAP诱导(- / -)和野生型(PACAP(+ / +))由K / BxN小鼠血清转移。疾病的一般特征进行了半定量的得分,plethysmometry和病理分析。机械和thermonociceptive阈值和运动功能评估。代谢活动被正电子发射断层扫描评估。骨形态被体内微型电脑断层扫描测量,髓过氧化物酶活性和过氧化物生产生物荧光成像与鲁米诺和lucigenin分别由荧光吲哚菁绿血管通透性染料的研究。结果:PACAP(+ / +)小鼠发展显著的关节肿胀,减少把握能力,和机械(但不是热)K / BxN血清转移后痛觉过敏。PACAP(- / -)小鼠临床分数和水肿明显减少,和机械痛觉过敏和运动损伤缺席,在两周的观察。代谢活动和过氧化物生产增加tibiotarsal关节的野生型老鼠,但显著低于PACAP(- / -)动物。 Myeloperoxidase activity in the ankle joints of PACAP(-/-) mice was significantly reduced in the early phase of arthritis, but increased in the late phase. Synovial hyperplasia was also significantly increased, and progressive bone spur formation was observed in PACAP-deficient mice only. CONCLUSION: In PACAP-deficient mice with serum-transfer arthritis, joint swelling, vascular leakage, hyperalgesia, and early inflammatory cell accumulation are reduced; in the later phase of the disease, immune cell function and bone neoformation are increased. Elucidation of the underlying pathways of PACAP activity may open promising new avenues for development of therapy in inflammatory arthritis.

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