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| 白细胞介素-17A在小鼠机械通气相关性肺损伤中的作用 |
| Role of interleukin-17A on ventilator-induced lung injury in mice |
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| DOI：10.12089/jca.2021.08.014 |
| 中文关键词: 白细胞介素-17A 机械通气 肺损伤 炎症反应 凋亡 |
| 英文关键词: Interleukin-17A Mechanical ventilation Lung injury Inflammatory reaction Apoptosis |
| 基金项目:国家自然科学基金面上项目（81571936） |
| 作者 | 单位 | E-mail | | 黄天丰 | 225001,扬州大学附属江苏省苏北人民医院麻醉科,扬州大学附属江苏省苏北人民医院麻醉与急危重症研究所 | | | 高巨 | 225001,扬州大学附属江苏省苏北人民医院麻醉科,扬州大学附属江苏省苏北人民医院麻醉与急危重症研究所 | gaoju_003@163.com | | 王存金 | 225001,扬州大学附属江苏省苏北人民医院麻醉科,扬州大学附属江苏省苏北人民医院麻醉与急危重症研究所 | | | 张扬 | 225001,扬州大学附属江苏省苏北人民医院麻醉科,扬州大学附属江苏省苏北人民医院麻醉与急危重症研究所 | | | 李勇 | 225001,扬州大学附属江苏省苏北人民医院麻醉科,扬州大学附属江苏省苏北人民医院麻醉与急危重症研究所 | | | 葛亚丽 | 225001,扬州大学附属江苏省苏北人民医院麻醉科,扬州大学附属江苏省苏北人民医院麻醉与急危重症研究所 | |
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| 中文摘要: |
目的 探讨白细胞介素-17A（IL-17A）在小鼠机械通气相关性肺损伤中的作用。
方法 SPF级雄性C57BL/6小鼠40只，2～3月龄，体重25～30 g。将小鼠随机分为四组：假手术组（S组），假手术+IL-17A单克隆抗体组（SA组），机械通气肺损伤模型组（V组），机械通气损伤模型+IL-17A单克隆抗体组（VA组），每组10只。S组和SA组仅行气管切开保留自主呼吸。V组和VA组机械通气4 h。SA组和VA组在气管切开后于腹腔注射IL-17A单克隆抗体（10 μg，0.1 ml），S组和V组于腹腔注射等体积的抗体稀释液。机械通气结束时处死小鼠取肺组织，采用ELISA法检测支气管肺泡灌洗液（BALF）中肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）浓度，测定肺组织湿干重比值（W/D），采用TUNEL染色法测定肺组织细胞凋亡指数，采用Western Blot法检测肺组织IL-17A和cleaved-caspase-3蛋白含量，采用HE染色法观察肺组织病理学
结果 并进行肺损伤评分。结果与S组比较，V组和VA组BALF中TNF-α和IL-6浓度、W/D、细胞凋亡指数、肺组织IL-17A和cleaved-caspase-3蛋白含量、肺损伤评分均明显升高（P<0.05），肺组织病理学改变加重。与V组比较，VA组BALF中TNF-α和IL-6浓度、W/D、细胞凋亡指数、肺组织IL-17A和cleaved-caspase-3蛋白含量、肺损伤评分均明显降低（P<0.05），肺组织病理学损伤改善。S组和SA组各项指标差异无统计学意义。
结论 大潮气量机械通气可导致机械通气相关性肺损伤，IL-17A介导了机械通气相关性肺损伤的发生、发展过程，可能与IL-17A加重炎症反应和诱导细胞凋亡有关。阻断IL-17A可通过减轻肺组织炎症反应、减少细胞凋亡改善机械通气相关性肺损伤。 |
| 英文摘要: |
Objective To evaluate the role of interleukin-17A on ventilator-induced lung injury in mice.
Methods Forty male SPF C57BL/6 mice, aged 2-3 months, were equally and randomly divided into 4 groups (n = 10) using a random number table: sham group (group S), sham + IL-17A antibody group (group SA), ventilator-induced lung injury group (group V), ventilator-induced lung injury + IL-17A antibody group (group VA). The mice were tracheostomized and spontaneous breathing was maintained in group S and group SA, while the other mice were tracheostomized and mechanically ventilated for 4 hour in group V and group VA. The mice in group SA and group VA were intraperitoneally injected with 10 μg/0.1 ml of IL-17A monoclonal antibody after tracheotomy, and the mice in group S and group V were given equal volume of antibody dilution as negative control. Animals were sacrificed at the end of mechanical ventilation, bronchoalveolar lavage fluid (BALF) was collected and ELISA method was used to detect tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) concentration, wet to dry weight ratio (W/D) was measured, apoptosis index was measured by TUNEL staining, IL-17A and cleaved-caspase-3 expression were detected by Western Blot . At last, pathological results were observed by HE staining and lung injury score was performed.
Results Compared with group S, TNF-α and IL-6 concentration in BALF, W/D, apoptosis index, and the expression of IL-17A and cleaved-caspase-3 protein in lung tissue and lung injury score were significantly increased in group V and group VA(P < 0.05), the lung histopathological changes were worse. Compared with group V, the concentration of TNF-α and IL-6 in BALF, W/D, apoptosis index, and the expression of IL-17A and cleaved-caspase-3 protein in lung tissue and lung injury scorewere significantly reduced in group VA (P < 0.05); and the pathological damage of lung tissue was improved. There was no statistically significant difference in indicators between group S and group SA.
Conclusion High tidal volume mechanical ventilation can lead to ventilator-induced lung injury. IL-17A mediates the occurrence and development of ventilator-induced lung injury, which may be related to IL-17A aggravating inflammation and inducing cell apoptosis. Blocking IL-17A can improve ventilator-induced lung injury by reducing the inflammatory response of lung tissue and reducing cell apoptosis. |
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