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首页> 外文期刊>American Journal of Physiology >Sex differences in inflammation and inflammatory pain in cyclooxygenase-deficient mice.
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Sex differences in inflammation and inflammatory pain in cyclooxygenase-deficient mice.

机译：环氧合酶缺乏症小鼠的炎症和炎性疼痛的性别差异。

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摘要

There are two cyclooxygenase (COX) genes encoding characterized enzymes, COX-1 and COX-2. Nonsteroidal anti-inflammatory drugs are commonly used as analgesics in inflammatory arthritis, and these often inhibit both cyclooxygenases. Recently, inhibitors of COX-2 have been used in the treatment of inflammatory arthritis, as this isoform is thought to be critical in inflammation and pain. The objective of this study was to determine the effect of COX-1 or COX-2 gene disruption on the development of chronic Freund's adjuvant-induced arthritis and inflammatory pain in male and female mice. The effect of COX-1 or COX-2 gene disruption on inflammatory hyperalgesia, allodynia, inflammatory edema, and arthritic joint destruction was studied. COX-2 knockout mice (COX-2-/-) showed reduced edema and joint destruction in female, but not male, animals. In addition, neither male nor female COX-2-/- mice developed thermal hyperalgesia or mechanical allodynia, either ipsilateral or contralateral to the inflammation. COX-1 gene disruption also reduced inflammatory edema and joint destruction in female, but not male mice, although females of both COX-/- lines did show some bony destruction. There was no difference in ipsilateral allodynia between COX-1 knockout and wild-type animals, but female COX-1-/- mice showed reduced contralateral allodynia compared with male COX-1-/- or wild-type mice. These data show that the gene products of both COX genes contribute to pain and local inflammation in inflammatory arthritis. There are sex differences in some of these effects, and this suggests that the effects of COX inhibitors may be sex dependent.
机译：有两种编码特征酶的环氧合酶（COX）基因：COX-1和COX-2。非甾体类抗炎药通常在炎性关节炎中用作镇痛药，并且通常会抑制两种环氧合酶。最近，COX-2抑制剂已被用于治疗炎症性关节炎，因为这种同工型被认为对炎症和疼痛至关重要。这项研究的目的是确定COX-1或COX-2基因破坏对雄性和雌性小鼠慢性弗氏佐剂诱发的关节炎和炎性疼痛的发展的影响。研究了COX-1或COX-2基因破坏对炎症性痛觉过敏，异常性疼痛，炎症性水肿和关节炎性关节破坏的影响。 COX-2基因敲除小鼠（COX-2-/-）在雌性动物而非雄性动物中表现出水肿减轻和关节破坏。此外，雄性和雌性COX-2-/-小鼠均未出现热痛觉过敏或机械性异常性疼痛，与炎症同侧或对侧。尽管两种COX-/-系的雌性确实表现出一定的骨质破坏，但COX-1基因的破坏也可减轻雌性小鼠的炎症性水肿和关节破坏，但不减少雄性小鼠。在COX-1基因敲除小鼠和野生型动物之间同侧异常性疼痛没有差异，但是与雄性COX-1-/-或野生型小鼠相比，雌性COX-1-/-小鼠的对侧异常性疼痛减少。这些数据表明，两种COX基因的基因产物都有助于炎性关节炎中的疼痛和局部炎症。这些影响中有些存在性别差异，这表明COX抑制剂的影响可能与性别有关。

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