DJ-X-013可降低LPS诱导的炎症,调节Th17/骨髓系衍生抑制细胞,并改变NF-κB表达,以改善实验性结肠炎
Mousumi Mandal1, Ahmed Rakib1, Md Abdullah Al Mamun1
1Department of Pharmaceutical Sciences, College of Pharmacy, The University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
|September 10, 2024
概括
新型化合物DJ-X-013在细胞模型中显示出抗炎作用,并在实验性结肠炎中减少炎症. 这种化合物可能为炎症性肠病 (IBD) 提供一种新的治疗策略.
科学领域:
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
- 药理学 药理学是指药理学的学科.
背景情况:
- 炎症性肠病 (IBD) 是一种与过度免疫反应相关的慢性疾病.
- IBD的病因在很大程度上仍未知,这推动了对新型治疗点的研究.
研究的目的:
- 研究新型化合物DJ-X-013.的抗炎性质.
- 评估DJ-X-013在体外和体内炎症模型中的疗效.
主要方法:
- 使用脂聚糖 (LPS) 激活的巨细胞 (体外) 和硫酸 (DSS) 诱导的大肠炎模型 (体内).
- 评估细胞形态,组织结构,细胞因子表达和免疫细胞群体,使用组织学,流细胞计,RT-qPCR,多重和免疫斑分析.
主要成果:
- DJ-X-013调节了巨细胞形态和抑制了炎症标志物,包括NF-κB.
- 在体内,DJ-X-013改善了体重,结肠长度,并减轻了结肠炎症.
- DJ-X-013增加了有益的免疫细胞 (MDSCs,DCs,NKTs),并减少了结肠膜自身中的炎症细胞 (中性粒细胞,TNF-α巨细胞,Th17细胞).
结论:
- 在实验模型中,DJ-X-013显示出显著的抗炎作用.
- 该化合物显示为改善炎症和结肠炎的治疗策略.
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