Department of Infectious Disease, Hospital of Chengdu University of Traditional Chinese Medicine, China.
Department of Infectious Disease, Chengdu First People's Hospital, Chengdu, Sichun, China.
Comput Math Methods Med. 2022 Sep 20;2022:8297046. doi: 10.1155/2022/8297046. eCollection 2022.
To investigate the regulatory role of angiopoietin-1ike protein 2 (Angptl 2) in the pathogenesis of acute respiratory distress syndrome (ARDS).
A high-fat diet (HFD) and tail vein injection of 0.1 ml/kg oleic acid were used to induce acute lung injury (ALI) and ARDS models, and male Kunming mice were randomly divided into four groups: control group (injected with normal saline), ALI group (injected with oleic acid), HFD group (injection of normal saline), and ARDS group (HFD+injection of oleic acid). The degree of lung injury was assessed by lung histopathology score and lung injury index. At the same time, the mRNA and protein expression levels of Angptl 2 in lung tissue were also detected to determine the relationship between Angptl 2 and ARDS.
Lee's index of the HFD group and ARDS group was significantly higher than that of the control group and ALI group ( < 0.05), and the lung injury index of the ARDS group was significantly higher than that of the ALI group. The expression of Angptl 2 in the lung tissue of the ALI group and ARDS group was significantly different, and the Angptl 2 mRNA level was the highest in the ARDS group. Immunohistochemistry showed that the alveolar walls of the ALI group and ARDS group were severely collapsed, and the ARDS group had the greatest Angptl 2 aggregation at the site of edema exudation.
Collectively, obesity might be mediated by Angptl 2 and promotes lung injury. Immunohistochemistry analysis showed that the expression of the receptor on alveolar walls was correlated with Angptl 2, which increased alveolar wall permeability, edema fluid exudation, and alveolar wall collapse. Thus, Angptl 2 might be a target for improving the treatment of ARDS.
研究血管生成素样蛋白 2(Angptl 2)在急性呼吸窘迫综合征(ARDS)发病机制中的调节作用。
采用高脂饮食(HFD)联合尾静脉注射 0.1ml/kg 油酸的方法诱导急性肺损伤(ALI)和 ARDS 模型,将雄性昆明小鼠随机分为 4 组:对照组(注射生理盐水)、ALI 组(注射油酸)、HFD 组(注射生理盐水)和 ARDS 组(HFD+注射油酸)。通过肺组织病理评分和肺损伤指数评估肺损伤程度。同时,检测肺组织中 Angptl 2 的 mRNA 和蛋白表达水平,以确定 Angptl 2 与 ARDS 的关系。
HFD 组和 ARDS 组的 Lee 指数明显高于对照组和 ALI 组( < 0.05),ARDS 组的肺损伤指数明显高于 ALI 组。ALI 组和 ARDS 组肺组织 Angptl 2 的表达存在显著差异,其中 ARDS 组 Angptl 2mRNA 水平最高。免疫组化结果显示,ALI 组和 ARDS 组的肺泡壁严重塌陷,ARDS 组在水肿渗出部位的 Angptl 2 聚集最多。
肥胖可能通过 Angptl 2 介导,促进肺损伤。免疫组化分析表明,肺泡壁上受体的表达与 Angptl 2 相关,增加了肺泡壁通透性、水肿液渗出和肺泡壁塌陷。因此,Angptl 2 可能是改善 ARDS 治疗的靶点。