Takagi Tomohisa, Naito Yuji, Inoue Mamoru, Akagiri Satomi, Mizushima Katsura, Handa Osamu, Kokura Satoshi, Ichikawa Hiroshi, Yoshikawa Toshikazu
Department of Molecular Gastroenterology and Hepatology, Graduate School of Medical Sience, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Inflammation. 2009 Apr;32(2):83-8. doi: 10.1007/s10753-009-9106-6.
Carbon monoxide (CO), long considered a toxic gas, has recently been shown to mediate anti-inflammatory effects in various animal models. The aim of this study was to investigate whether the inhalation of CO ameliorated collagen-induced arthritis (CIA) in mice. CIA was induced in female DBA/1 mice by the injection of an anti-type II collagen antibody and lipopolysaccharide. The CO treatment group was exposed to CO gas at a concentration of 200 ppm in a closed cage starting on the day of the injection with an anti-type II collagen antibody and throughout the remaining study period. The clinical arthritis scores was examined daily for swelling of the paws as a sign of arthritis. For histopathology, the sections of the hind legs were evaluated by hematoxylin-eosin staining. Moreover, we evaluated the expression of interleukin (IL)-1beta and monocyte chemoattractant protein-1 (MCP-1) mRNA in the hind paws. Both clinical arthritis scores as well as histological findings of joint inflammation were significantly reduced in mice treated with CO gas inhalation compared to untreated mice. Further, CO significantly inhibited the increased expression of IL-1beta and MCP-1 mRNA in paws at day 3 after the induction of arthritis. In conclusion, the inhalation of CO protected mice from the synovial inflammation of CIA. Based on these data, the beneficial effects of CO in murine RA model may be attributed to its anti-inflammatory properties.
一氧化碳（CO）长期以来被视为一种有毒气体，最近的研究表明它在多种动物模型中具有介导抗炎作用。本研究的目的是探讨吸入CO是否能改善小鼠胶原诱导性关节炎（CIA）。通过注射抗II型胶原抗体和脂多糖在雌性DBA/1小鼠中诱导CIA。从注射抗II型胶原抗体当天开始，CO治疗组在封闭笼中暴露于浓度为200 ppm的CO气体中，并持续整个剩余研究期。每天检查临床关节炎评分，以爪部肿胀作为关节炎的标志。对于组织病理学，通过苏木精-伊红染色评估后腿切片。此外，我们评估了后爪中白细胞介素（IL）-1β和单核细胞趋化蛋白-1（MCP-1）mRNA的表达。与未处理的小鼠相比，吸入CO气体处理的小鼠临床关节炎评分以及关节炎症的组织学结果均显著降低。此外，CO在关节炎诱导后第3天显著抑制了爪中IL-1β和MCP-1 mRNA表达的增加。总之，吸入CO可保护小鼠免受CIA的滑膜炎症。基于这些数据，CO在小鼠类风湿性关节炎模型中的有益作用可能归因于其抗炎特性。
