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Role of cyclooxygenase isoforms in the altered excitatory motor pathways of human colon with diverticular disease

机译：环氧合酶亚型在人结肠憩室疾病兴奋性运动通路改变中的作用

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BACKGROUND AND PURPOSE: The COX isoforms (COX-1, COX-2) regulate human gut motility, although their role under pathological conditions remains unclear. This study examines the effects of COX inhibitors on excitatory motility in colonic tissue from patients with diverticular disease (DD).\udEXPERIMENTAL APPROACH: Longitudinal muscle preparations, from patients with DD or uncomplicated cancer (controls), were set up in organ baths and connected to isotonic transducers. Indomethacin (COX-1/COX-2 inhibitor), SC-560 (COX-1 inhibitor) or DFU (COX-2 inhibitor) were assayed on electrically evoked, neurogenic, cholinergic and tachykininergic contractions, or carbachol- and substance P (SP)-induced myogenic contractions. Distribution and expression of COX isoforms in the neuromuscular compartment were assessed by RT-PCR, Western blot and immunohistochemical analysis.\udKEY RESULTS: In control preparations, neurogenic cholinergic contractions were enhanced by COX inhibitors, whereas tachykininergic responses were blunted. Carbachol-evoked contractions were increased by indomethacin or SC-560, but not DFU, whereas all inhibitors reduced SP-induced motor responses. In preparations from DD patients, COX inhibitors did not affect electrically evoked cholinergic\udcontractions. Both indomethacin and DFU, but not SC-560, decreased tachykininergic responses. COX inhibitors did not modify carbachol-evoked motor responses, whereas they counteracted SP-induced contractions. COX-1 expression was decreased in myenteric neurons, whereas COX-2 was enhanced in glial cells and smooth muscle.\udCONCLUSIONS AND IMPLICATIONS: In control colon, COX-1 and COX-2 down-regulate cholinergic motility, whereas both isoforms enhance tachykininergic motor activity. In the presence of DD, there is a loss of modulation by both COX isoforms on the cholinergic system, whereas COX-2 displays an enhanced\udfacilitatory control on tachykininergic contractile activity.
机译：背景和目的：尽管尚不清楚在病理条件下它们的作用，但COX亚型（COX-1，COX-2）调节人的肠蠕动。这项研究检查了COX抑制剂对憩室病（DD）患者结肠组织兴奋性运动的影响。\实验方法：将DD或未患癌症的患者（对照）的纵向肌肉制剂放在器官浴中并连接等渗换能器消炎痛（COX-1 / COX-2抑制剂），SC-560（COX-1抑制剂）或DFU（COX-2抑制剂）在电诱发的，神经源性的，胆碱能的和速激肽能的收缩或卡巴胆碱和物质P（SP ）引起的肌源性收缩。通过RT-PCR，Western印迹和免疫组化分析评估了COX亚型在神经肌肉区中的分布和表达。\ ud关键结果：在对照制剂中，COX抑制剂可增强神经源性胆碱能收缩，而速激肽反应则较钝。吲哚美辛或SC-560会增加卡巴胆碱引起的收缩，但DFU不会，而所有抑制剂均会降低SP诱导的运动反应。在DD患者的制剂中，COX抑制剂不影响电诱发的胆碱能/非收缩。消炎痛和DFU均可，但SC-560则不会降低速激肽能反应。 COX抑制剂不会改变卡巴胆碱引起的运动反应，而可以抵消SP引起的收缩。结论：在对照结肠中，COX-1和COX-2下调胆碱能运动性，而这两种同工型均能提高速激肽能动性。\ ud结论和含义：在对照结肠中，COX-1和COX-2下调胆碱能运动性。运动活动。在DD的存在下，胆碱能系统的两种COX同工型均失去调节作用，而COX-2则表现出对速激肽能收缩活性的增强/不利控制。

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