Xing Runlin, Wang Peimin, Zhao Linrui, Xu Bo, Zhang Nongshan, Li Xiaochen
Department of Orthopedic, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Arch Rheumatol. 2017 Jan 18;32(2):96-104. doi: 10.5606/ArchRheumatol.2017.6061. eCollection 2017 Jun.
This study aims to observe both transient receptor potential ankyrin 1 (TRPA1) and transient receptor potential vanilloid 4 (TRPV4) expressions in synovial tissues of rats with mechanical hyperalgesia induced by experimental knee osteoarthritis (KOA).
Forty-five four-month-old Sprague Dawley male rats, weight ranging from 440 g to 470 g, were randomly allocated into three groups, namely KOA group, KOA-antagonist group, and normal group. Mechanical withdrawal thresholds of five rats from each group were detected one week before modeling, and two, four, six, and eight weeks after modeling, respectively. Synovial and cartilage tissues from diseased knee were collected after sacrificing the rats eight weeks after modeling so to observe pathological morphology at cartilage tissues and to determine protein and gene expressions of TRPA1 and TRPV4 at synovial tissues.
Rats with KOA showed obvious mechanical hyperalgesia from two weeks after modeling to the latest follow-up, eight weeks after modeling. The abnormally low level of mechanical withdrawal thresholds can be increased by TRPA1 and TRPV4 ion channel blockers.
Up-regulating expressions of TRPA1 and TRPV4 participate in the occurrence mechanism of mechanical hyperalgesia induced by KOA.
本研究旨在观察实验性膝骨关节炎（KOA）诱导的机械性痛觉过敏大鼠滑膜组织中瞬时受体电位锚蛋白1（TRPA1）和瞬时受体电位香草酸受体4（TRPV4）的表达。
45只4月龄、体重440 g至470 g的雄性Sprague Dawley大鼠被随机分为三组，即KOA组、KOA拮抗剂组和正常组。在建模前一周以及建模后2周、4周、6周和8周分别检测每组5只大鼠的机械性撤针阈值。建模8周后处死大鼠，收集患病膝关节的滑膜和软骨组织，以观察软骨组织的病理形态，并测定滑膜组织中TRPA1和TRPV4的蛋白质和基因表达。
KOA大鼠从建模后2周直至建模后8周的最新随访期间均表现出明显的机械性痛觉过敏。TRPA1和TRPV4离子通道阻滞剂可提高异常降低的机械性撤针阈值。
TRPA1和TRPV4表达上调参与了KOA诱导的机械性痛觉过敏的发生机制。
