Role of intestinal macrophages in the pathogenesis of intestinal lesions induced by non-steroidal anti-inflammatory drugs.

肠道巨噬细胞在非甾体抗炎药所致肠道病变发病机制中的作用。

• 批准号: 20590550
• 负责人: KATO Shinichi
• 金额: $ 3万
• 依托单位: Kyoto Pharmaceutical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20590550/
• 关键词: 非ステロイド性抗炎症薬(NSAID); マクロファージ; 消化管傷害; α7ニコチン性アセチルコリン受容体; 内皮型NO合成酵素; 一酸化窒素(NO); 消化管マクロファージ; 内皮型NO合成酵素(eNOS); 一酸化窒素; α7ニコチンアセチルコリン受容体; 腸管マクロファージ; 小腸障害傷害; 誘導型NO合成酵素(iNOS); 非ステロイド性抗炎症薬(NSAID); マクロファージ; 消化管傷害; α7ニコチン性アセチルコリン受容体; 内皮型NO合成酵素; 一酸化窒素(NO); 消化管マクロファージ; 内皮型NO合成酵素(eNOS); 一酸化窒素; α7ニコチンアセチルコリン受容体; 腸管マクロファージ; 小腸障害傷害; 誘導型NO合成酵素(iNOS)

In the present study, we investigated the role intestinal macrophages in the pathogenesis of gastrointestinal diseases.1. The activation of α7 nicotinic acetylcholine receptor (α7nAChR) suppresses the severity of intestinal lesions induced by non-steroidal anti-inflammatory drugs (NSAID).2. Dopamine D2 receptor antagonists significantly prevent NSAID-induced intestinal lesions through activation ofα7nAChR.3. The aggravation of NSAID-induced gastric damage during arthritis is attributable to the upregulation of iNOS and eNOS.4. Lansoprazole, a proton pump inhibitor, protects NSAID-induced intestinal lesions through induction of heme oxygenase (HO)-1.5. Macrophages play a beneficial role in the healing of chronic gastric ulcers mediated by increase in neovascularization through upregulation of cyclooxygenase (COX)-2 and vascular endothelial growth factor (VEGF).

在本研究中，我们研究了肠道巨噬细胞在胃肠道疾病的发病机理中的作用。1。 α7烟碱乙酰胆碱受体（α7NACHR）的激活抑制了非甾体类抗炎药（NSAID）诱导的肠道病变的严重程度.2。多巴胺D2受体拮抗剂可通过激活α7nAChr.3显着防止NSAID诱导的肠道病变。 NSAID引起的关节炎期间NSAID诱导的胃损伤的聚集归因于Inos和Enos的上调4。质子泵抑制剂Lansoprazole通过诱导血红素加氧酶（HO）-1.5来保护NSAID诱导的肠道病变。巨噬细胞通过上调环氧酶（COX）-2和血管内皮生长因子（VEGF）的上调，通过增加新血管形成介导的慢性胃溃疡的愈合中起着有益的作用。