摘要/Abstract
摘要： 目的 ·探讨胰岛素样生长因子 1（insulin-like growth factor 1，IGF-1）对小鼠肺泡上皮细胞株 MLE-12细胞吞噬功能和白细胞介素 10（interleukin-10，IL-10）产生的影响。方法 ·体外培养的 MLE-12细胞，在有或无磷脂酰肌醇 -3-激酶（ phosphatidylinositol3-kinase，PI3K）抑制剂 wortmannin存在下用 IGF-1刺激 48 h；加入荧光微球孵育 2 h后，流式细胞术检测细胞吞噬荧光微球情况。酶联免疫吸附试验检测 IGF-1刺激 MLE-12细胞 24 h后上清液中 IL-10的含量。 IGF-1预处理 2 h后，脂多糖（ lipopolysaccharides， LPS）刺激 MLE-12细胞 24 h，Western blotting检测细胞质中磷酸化信号转导与转录激活因子 3（phosphorylated signal transduction and activator of transcription 3，p-STAT3）的表达情况。结果 ·随着 IGF-1刺激浓度的增加， MLE-12细胞吞噬荧光微球的能力增强；在 50 ng/mL的 IGF-1的刺激下， MLE-12细胞吞噬荧光微球的能力达到峰值。 wortmannin阻断 PI3K/蛋白激酶 B（Akt）途径， IGF-1促进 MLE-12细胞吞噬荧光微球的能力消失。 IGF-1促进 MLE-12细胞分泌 IL-10并抑制 LPS诱导的 STAT3激活。结论 · IGF-1通过 PI3K/Akt途径促进 MLE-12细胞的吞噬作用，并具有一定的抗炎作用。
关键词: 胰岛素样生长因子 1, MLE-12细胞, 吞噬功能, 白细胞介素 10, 信号转导与转录激活因子 3
Abstract:
Objective · To investigate the effect of insulin-like growth factor 1 (IGF-1) on phagocytosis and production of interleukin-10 (IL-10) in the murine alveolar epithelial cell line MLE-12. Methods · After treatment with IGF-1 for 48 h, MLE-12 cells were incubated with fluorescent microspheres for 2 h in the presence or absence of wortmannin (phosphatidylinositol-3-kinase inhibitor). Flow cytometry was then used to assess cell phagocytosis of fluorescent microspheres. Enzyme linked immunosorbent assay (ELISA) was used to detect the content of IL-10 in MLE-12 cells culture supernatant stimulatedIGF-1 for 24 h. After pretreatment with IGF-1 for 2 h, MLE-12 cells were stimulatedlipopolysaccharides (LPS) for 24 h, and the of phosphorylated signal transduction and activator of transcription 3 (p-STAT3) in cytoplasm was detectedWestern blotting. Results · With the increase of IGF-1 stimulation concentration, the ability of MLE-12 cells to phagocytose fluorescent microspheres increased, and the ability to phagocytose fluorescent microspheres reached the peak in the presence of IGF-1 at 50 ng/mL. However, the ability of IGF-1 to phagocytose fluorescent microspheres was completely blockedwortmannin in MLE-12 cells. IGF-1 promoted IL-10 secretion and inhibited LPS-induced enhancement of STAT3 activation in MLE-12 cells. Conclusion · IGF-1 promotes phagocytosis of MLE-12 cells via the PI3K/protein kinase B (Akt) pathway and exhibits anti-inflammatory properties.
Key words: insulin-like growth factor 1 (IGF-1), MLE-12 cell, phagocytosis, interleukin-10 (IL-10), signal transduction and activator of transcription 3 (STAT3)
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