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目的:探讨Gln对内毒素(LPS)诱导的大鼠肺泡Ⅱ型上皮细胞肿瘤坏死因子(TNF)-α表达和NF-κB活性的影响。方法:原代培养大鼠肺泡Ⅱ型上皮细胞,分为0、0.5、2.0、10.0 mmol/L Gln及10 mmol/L Gln、空白对照共六个组,作用8 h后,前四组1μg/mL LPS刺激24 h。用ELISA法测定细胞上清TNF-α的水平,电泳迁移率改变试验(EMSA)检测细胞内NF-κB活性。结果:Gln预处理可降低LPS诱导大鼠肺泡Ⅱ型上皮细胞TNF-α的表达,并且其作用呈剂量依赖性,在10 mmol/L浓度最为显著;Gln预处理对NF-κB活性有明显地抑制作用。结论:Gln预处理可抑制NF-κB活性,并降低LPS诱导的大鼠肺泡Ⅱ型上皮细胞TNF-α的表达,从而起到免疫调节的作用。
Objective: To investigate the effect of Gln on the expression of tumor necrosis factor (TNF) -α and the activity of NF-κB in rat alveolar type Ⅱ epithelial cells induced by endotoxin (LPS). Methods: Primary cultured rat alveolar type Ⅱ epithelial cells were divided into 0, 0.5, 2.0, 10.0 mmol / L Gln and 10 mmol / L Gln. Six blank control groups were established. After 8 h, mL LPS for 24 h. The level of TNF-α in the supernatant of the cells was measured by ELISA. The activity of NF-κB in the cells was detected by electrophoretic mobility shift assay (EMSA). Results: Gln preconditioning could reduce the TNF-α expression in LPS-induced rat alveolar type Ⅱ epithelial cells in a dose-dependent manner, especially at the concentration of 10 mmol / L. Gln pretreatment significantly increased the activity of NF-κB Inhibition. CONCLUSION: Gln pretreatment can inhibit the activity of NF-κB and decrease the expression of TNF-α induced by LPS in rat alveolar type Ⅱ epithelial cells, which play an immunomodulatory role.