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

在本研究中，我们探讨了肠道巨噬细胞在胃肠道疾病发病机制中的作用。α7烟碱乙酰胆碱受体（α7nAChR）的激活可抑制非甾体抗炎药（NSAID）诱导的肠道病变的严重程度。多巴胺D2受体拮抗剂通过激活α 7nachr .3显著预防nsaid诱导的肠道病变。关节炎期间nsaid引起的胃损伤加重可归因于iNOS和enos的上调。兰索拉唑是一种质子泵抑制剂，通过诱导血红素加氧酶(HO)-1.5来保护非甾体抗炎药诱导的肠道病变。巨噬细胞通过上调环氧化酶(COX)-2和血管内皮生长因子（VEGF）来增加新生血管，从而在慢性胃溃疡的愈合中发挥有益作用。

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).