在实验性严重喘和急性肺损伤中准常见的炎症媒介
Andrei Gheorghe Vicovan1, Diana Cezarina Petrescu1, Aurelia Cretu1
1Department of Morpho-Functional Sciences II-Pharmacology and Clinical Pharmacology, Faculty of Medicine, Grigore T. Popa University of Medicine and Pharmacy of Iasi, 16 Universitatii Street, 700115 Iasi, Romania.
在喘和急性肺损伤 (ALI) 的小鼠模型中,secukinumab (SECU) 和dexamethasone (DEXA) 调节炎症反应. 这两种治疗都降低了介质蛋白-17 (IL-17) 水平,表明了潜在的治疗益处.
科学领域:
- 免疫学 免疫学 免疫学
- 呼吸系统医学 呼吸系统医学
- 药理学 药理学是指药理学的学科.
背景情况:
- 中性粒细胞和干白素-17 (IL-17) 通过促进氧化应激,驱动严重的喘和急性肺损伤 (ALI).
- 用脂多糖化物 (LPS) 加重的卵胺诱导喘模型用于模仿严重的呼吸系统疾病.
研究的目的:
- 为了评估Secukinumab (SECU) 与甲 (DEXA) 相比的疗效,在ALI叠加于恶化喘的小鼠模型中.
- 研究SECU和DEXA对与Th1,Th2和Th17免疫反应相关的细胞因子概况的影响.
主要方法:
- 卵胺诱导的喘模型在小鼠中,加剧LPS诱导ALI.
- 使用塞库金纽马布 (SECU) 和甲 (DEXA) 的治疗.
- 在支气管洗液 (BALF) 和肺组织同质物中分析细胞因子水平 (TNF-α,IFN-γ,IL-6,IL-4,IL-5,IL-13,IL-17).
主要成果:
- 无论是SECU还是DEXA,都显著降低了干扰素- (IFN-γ),干扰素-6 (IL-6) 和干扰素-17 (IL-17) 的水平.
- DEXA增加了瘤坏死因子-α (TNF-α) 和Th2细胞因子 (IL-4,IL-5,IL-13),而SECU抑制了IL-5.
- 肺组织中的细胞因子变化通常与在BALF.中观察到的变化相似.
结论:
- 塞库金纽马布 (SECU) 显示出调节炎性细胞因子释放的能力,特别是减少Th17反应.
- SECU显示出作为治疗急性肺损伤和喘加剧的条件的治疗剂的潜力.
- SECU和DEXA都有效地降低了IL-17,这是一种关键的细胞因子,与严重喘和ALI的发病有关.
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