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目的:观察氧化低密度脂蛋白(ox-LDL)是否可以诱导血管平滑肌细胞(VSMCs)表达胸腺基质淋巴细胞生成素(TSLP),并探讨核因子-κB(NF-κB)信号通路在其中的作用。方法:原代培养VSMCs,分别用ox-LDL及ox-LDL联合NF-κB特异性抑制剂——吡咯烷二硫代氨基甲酸盐(PDTC)干预。采用免疫组织化学染色检测胞质中TSLP的表达,用ELISA法检测细胞培养上清液中TSLP的浓度,用电泳迁移率实验检测NF-κB的结合活性。结果:正常未经ox-LDL刺激的VSMCs几乎不表达TSLP,经ox-LDL刺激后胞质及上清液中的TSLP表达明显增加,并有浓度和时间依赖性。Ox-LDL刺激VSMCs表达TSLP的同时NF-κB信号通路激活,经PDTC预处理后TSLP表达量显著减少。结论:Ox-LDL能够诱导VSMCs表达TSLP,其作用机制可能为上调NF-κB的结合活性。
AIM: To investigate whether ox-LDL can induce the expression of TSLP in vascular smooth muscle cells (VSMCs) and to explore the role of NF-κB signaling pathway in it . Methods: Primary cultured VSMCs were treated with ox-LDL and ox-LDL in combination with pyrrolidine dithiocarbamate (PDTC), a specific inhibitor of NF-κB. The expression of TSLP in the cytoplasm was detected by immunohistochemical staining. The concentration of TSLP in the cell culture supernatant was detected by ELISA, and the binding activity of NF-κB was detected by electrophoretic mobility shift assay. Results: TSLP was almost not expressed in normal VSMCs stimulated by ox-LDL. The expression of TSLP in cytoplasm and supernatant stimulated by ox-LDL increased significantly and in a time-and concentration-dependent manner. Ox-LDL stimulated the VSMCs to express TSLP, meanwhile NF-κB signaling pathway was activated. After pretreatment with PDTC, TSLP expression was significantly reduced. CONCLUSION: Ox-LDL can induce VSMCs to express TSLP, and its mechanism may be up-regulated NF-κB binding activity.