Das Undurti N
UND Life Sciences, 2020 S 360th St, # K-202, Federal Way, WA, 98003, USA.
BioScience Research Centre and Department of Medicine, GVP Hospital, Gayatri Vidya Parishad College of Engineering Campus, Madhurawada, Visakhapatnam, 530 048, India.
Lipids Health Dis. 2016 Jan 13;15:11. doi: 10.1186/s12944-015-0165-4.
The inflammatory process seen in inflammatory bowel disease (IBD) is due to excess production of pro-inflammatory cytokines interleukin-1 (IL-1), IL-6, tumor necrosis factor-α (TNF-α), interferons (IFNs), macrophage migration inhibitory factor (MIF), HMGB1 (high mobility group B1) and possibly, a reduction in anti-inflammatory cytokines IL-10, IL-4, and transforming growth factor-β (TGF-β). These pro-inflammatory molecules lead to increased production of reactive oxygen species (ROS) including nitric oxide resulting in target tissue damage. I propose that inadequate production of inflammation resolving molecules lipoxins, resolvins, protectins, maresins and nitrolipids that suppress inflammation, ROS production, enhance wound healing and have cytoprotective properties results in inappropriate inflammation, delay in healing/repair process and so target tissue/organ damage continues in IBD. Hence, suggested therapeutic approach could include administration of stable synthetic analogues of lipoxins, resolvins, protectins, maresins and nitrolipids. This implies that measuring urine, stool and plasma levels of lipoxins, resolvins, protectins, maresins and nitrolipids may be used to detect the onset, progression and response to treatment of IBD.
炎症性肠病(IBD)中所见的炎症过程是由于促炎细胞因子白细胞介素-1(IL-1)、IL-6、肿瘤坏死因子-α(TNF-α)、干扰素(IFN)、巨噬细胞迁移抑制因子(MIF)、高迁移率族蛋白B1(HMGB1)产生过多,以及抗炎细胞因子IL-10、IL-4和转化生长因子-β(TGF-β)可能减少所致。这些促炎分子导致包括一氧化氮在内的活性氧(ROS)生成增加,从而造成靶组织损伤。我认为,抑制炎症、ROS生成、促进伤口愈合并具有细胞保护特性的炎症消退分子脂氧素、消退素、保护素、maresin和硝基脂质生成不足,导致IBD中出现不适当的炎症、愈合/修复过程延迟,进而靶组织/器官损伤持续存在。因此,建议的治疗方法可包括给予脂氧素、消退素、保护素、maresin和硝基脂质的稳定合成类似物。这意味着检测尿液、粪便和血浆中脂氧素、消退素、保护素、maresin和硝基脂质的水平,可用于检测IBD的发病、进展及对治疗的反应。