Department of Emergency Anesthesia, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China (mainland).
Med Sci Monit. 2018 Apr 20;24:2404-2412. doi: 10.12659/msm.906016.
BACKGROUND Acute lung injury (ALI) is responsible for mortality in hospitalized patients. Autophagy can negatively regulate inflammatory response, and CXCL16 (chemokine (C-X-C motif) ligand 16) is a kind of chemokine, which is closely related to the inflammatory response. However, the relationship between autophagy and CXCL16 in ALI is still unclear. This study aimed to investigate the role of autophagy and chemokine CXCL16 in ALI in mice. MATERIAL AND METHODS Thirty-two male C57BL/6 mice were divided into four groups. The control group (C group) was given normal saline through intraperitoneal injection. The L group was given LPS (lipopolysaccharide) at 30 mg/kg to construct an ALI model. The 3-MA group received an intraperitoneal injection of inhibitor of autophagy 3-methyladenine at 15 mg/kg, 30 minutes before LPS injection. The anti-CXCL16 group was given 20 mg/kg of CXCL16 monoclonal antibody 30 minutes before the LPS injection. RESULTS In the 3-MA Group, the level of histological analysis, lung wet/dry ratio, total protein of BAL (bronchoalveolar lavage fluid) and TNF-a level were higher than the L group (p<0.05), the level of autophagy was lower than the L group (p<0.05), and the level of CXCL16 was higher than the L group (p<0.05). In the anti-CXCL16 group, the level of histological analysis, lung wet/dry ratio, BAL protein, and TNF-α level were declined compared to the L group (p<0.05), but there was no statistically significant difference in expression of CXCL16 detected by ELISA between the anti-CXCL16 group and the L group (p>0.05). CONCLUSIONS Autophagy played a protective role in ALI induced by LPS in mice. Autophagy could regulate the level of CXCL16. The chemokine CXCL16 could exacerbate ALI.
急性肺损伤（ALI）是住院患者死亡的原因。自噬可以负向调节炎症反应，趋化因子（C-X-C 基序）配体 16（CXCL16）是一种趋化因子，与炎症反应密切相关。然而，自噬与 ALI 中 CXCL16 的关系尚不清楚。本研究旨在探讨自噬和趋化因子 CXCL16 在小鼠 ALI 中的作用。
32 只雄性 C57BL/6 小鼠随机分为 4 组。对照组（C 组）给予腹腔注射生理盐水。L 组给予 LPS（脂多糖）30mg/kg 构建 ALI 模型。3-MA 组在 LPS 注射前 30 分钟给予自噬抑制剂 3-甲基腺嘌呤 15mg/kg 腹腔注射。抗-CXCL16 组在 LPS 注射前 30 分钟给予 CXCL16 单克隆抗体 20mg/kg。
在 3-MA 组，组织学分析水平、肺湿/干重比、BAL（支气管肺泡灌洗液）总蛋白和 TNF-α 水平均高于 L 组（p<0.05），自噬水平低于 L 组（p<0.05），CXCL16 水平高于 L 组（p<0.05）。在抗-CXCL16 组，与 L 组相比，组织学分析水平、肺湿/干重比、BAL 蛋白和 TNF-α 水平均降低（p<0.05），但 ELISA 检测抗-CXCL16 组与 L 组之间 CXCL16 的表达无统计学差异（p>0.05）。
自噬在 LPS 诱导的小鼠 ALI 中发挥保护作用。自噬可以调节 CXCL16 的水平。趋化因子 CXCL16 可加重 ALI。
