Department of Anesthesiology, the First Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Department of Anesthesiology, the First Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Life Sci. 2020 Oct 15;259:118249. doi: 10.1016/j.lfs.2020.118249. Epub 2020 Aug 13.
We aimed to evaluate the effect of Dexmedetomidine (Dex) on immunology function of macrophages and inflammatory reactions in non-ventilated lung tissues from both humans and rats.
Patients scheduled for lung lobectomy were randomly assigned to traditional anesthesia group or Dex anesthesia group, 15 subjects in each group. CD68, CD86 and CD206 were used to mark activate and polarized macrophages using immunofluorescence staining in human lung tissues. Sprague-Dawley rats were used to set lung injury model and randomly divided into Control group, one-lung ventilation group (CLI group) and CLI + Dex group. Lung tissues and bronchoalveolar lavage fluid (BALF) from non-ventilated lungs were collected. The acquired lung tissues were subjected to hematoxylin-eosin (H&E) staining and the inflammatory cells in BALF were calculated. Levels of cytokines and chemokines were detected by enzyme-linked immunosorbent assays (ELISA).
Results from humans showed that anesthesia with Dex decreased the number of both CD68 positive cells and CD86 positive cells and down-regulated level of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and monocyte chemotactic protein 1 (MCP-1) in human lung. Results from rats demonstrated that treatment with Dex reversed the increased inflammatory cells in lung and the increased levels of TNF-α, interleukin-1β (IL-β), MCP-1 and chemokine (C-X-C motif) ligand 1 (CXCL1) resulted from non-ventilation; Dex increased the anti-inflammatory cytokine interleukin-10 (IL-10) in BALF from non-ventilated lung.
This study showed that Dex modulated the activation and immunological function of macrophages in non-ventilated lung and revealed a protective role in collapsed lung injury.
本研究旨在评估右美托咪定（Dex）对人类和大鼠非通气肺组织中巨噬细胞免疫功能和炎症反应的影响。
拟行肺叶切除术的患者被随机分为传统麻醉组或 Dex 麻醉组，每组 15 例。采用免疫荧光染色法，用 CD68、CD86 和 CD206 标记激活和极化的巨噬细胞。使用 Sprague-Dawley 大鼠建立肺损伤模型，并随机分为对照组、单肺通气组（CLI 组）和 CLI+Dex 组。收集非通气肺的肺组织和支气管肺泡灌洗液（BALF）。对获取的肺组织进行苏木精-伊红（H&E）染色，并计算 BALF 中的炎症细胞。通过酶联免疫吸附试验（ELISA）检测细胞因子和趋化因子水平。
来自人类的研究结果表明，Dex 麻醉可减少 CD68 阳性细胞和 CD86 阳性细胞的数量，并下调人类肺组织中促炎细胞因子肿瘤坏死因子-α（TNF-α）和单核细胞趋化蛋白 1（MCP-1）的水平。来自大鼠的研究结果表明，Dex 治疗可逆转非通气引起的肺炎症细胞增加以及 TNF-α、白细胞介素-1β（IL-β）、MCP-1 和趋化因子（C-X-C 基序）配体 1（CXCL1）水平升高；Dex 增加了非通气肺 BALF 中的抗炎细胞因子白细胞介素-10（IL-10）。
本研究表明 Dex 调节了非通气肺中巨噬细胞的激活和免疫功能，并在萎陷肺损伤中发挥了保护作用。
