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苗润新.左氧氟沙星通过下调核苷酸结合寡聚化结构域2抑制脂多糖诱导的肺泡上皮细胞凋亡及炎性反应[J].内科急危重症杂志,2025,31(3):271-274
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| DOI：10.11768/nkjwzzzz20250316 |
| 中文关键词: 左氧氟沙星 核苷酸结合寡聚化结构域2 肺炎 凋亡 炎性因子 |
| 英文关键词: |
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| 摘要点击次数: 270 |
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| 中文摘要: |
| 摘要 目的：探讨左氧氟沙星对脂多糖（LPS）诱导的人肺泡上皮细胞凋亡及炎性因子表达的影响及其对核苷酸结合寡聚化结构域2（NOD2）的调控作用。方法：体外培养肺泡上皮细胞，使用浓度为15 μg/mL的LPS处理24 h，设置实验1、2、3组（左氧氟沙星分别为0.3、0.6、0.9 μmol/mL与LPS共同处理细胞24 h）。流式细胞术检测细胞凋亡率；酶联免疫吸附试验（ELISA）检测白介素（IL）-10、肿瘤坏死因子（TNF）-α、IL-18的水平；NOD2过表达后，采用上述方法检测细胞凋亡率及IL-10、TNF-α、IL-18水平；蛋白免疫印迹法（WB）检测天冬氨酸特异性的半胱氨酸蛋白水解酶3（caspase 3）、裂解的caspase 3（cleaved-caspase 3）、NOD2的表达量。结果：LPS诱导后与对照组比较，模型组细胞凋亡率、caspase 3、cleaved-caspase 3、NOD2蛋白水平、TNF-α及IL-18水平升高，而IL-10水平降低（P均＜0.05）；0.3 μmol/mL（实验1组）、0.6 μmol/mL（实验2组）、0.9 μmol/mL（实验3组）左氧氟沙星可明显降低LPS诱导的细胞凋亡率、caspase 3、cleaved-caspase 3、NOD2蛋白水平、TNF-α及IL-18水平，而提高IL-10水平（P均＜0.05）。NOD2过表达可明显降低0.9 μmol/mL左氧氟沙星对肺泡上皮细胞凋亡及炎性反应的作用。结论：左氧氟沙星可能通过调控NOD2的表达抑制肺泡上皮细胞凋亡及炎性反应。 |
| 英文摘要: |
| Objective: To investigate the effect of levofloxacin on lipopolysaccharide (LPS)-induced alveolar epithelial cell apoptosis and expression of inflammatory factors and its regulatory effect on nucleotide-binding oligomerization domain 2 (NOD2). Methods: Alveolar epithelial cells were cultured in vitro, and treated with LPS at a concentration of 15μg/mL for 24h. The experiment set up the experimental group 1, experimental group 2 and the experimental group 3 (the cells were treated with 0.3, 0.6, 0.9μmol/mL levofloxacin and LPS for 24h, respectively). Flow cytometry was used to detect the apoptotic rate. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleukin (IL)-10, tumor necrosis factor (TNF)-α and IL-18. After NOD2 overexpression, the apoptosis rate and the levels of IL-10, TNF-α, and IL-18 were detected by the above methods. Western blotting was used to detect the expression of cysteinyl aspartate specific proteinase 3 (caspase 3), cleaved cysteinyl aspartate specific proteinase 3 (cleaved-caspase 3) and NOD2. Results: After LPS induction, compared with control group, the apoptosis rate, the protein levels of caspase 3, cleaved-caspase 3, NOD2, and the levels of TNF-α and IL-18 were increased in the model group, while the level of IL-10 was decreased (all P< 0.05). 0.3μmol/mL (experimental group 1), 0.6 μmol/mL (experimental group 2), 0.9 μmol/mL (experimental group 3) levofloxacin could significantly reduce the LPS-induced apoptosis rate, the protein levels of caspase 3, cleaved-caspase 3, NOD2, and the levels of TNF-α and IL-18, while increase the level of IL-10 (all P< 0.05). Overexpression of NOD2 could significantly reduce the effect of 0.9μmol/mL levofloxacin on the apoptosis and inflammatory response of alveolar epithelial cells. Conclusion: Levofloxacin may inhibit alveolar epithelial cell apoptosis and inflammatory response by regulating the expression of NOD2. |
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