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目的研究罗勒多糖抑制转化生长因子-β(TGF-β)诱导的A549细胞上皮间质转化的作用,揭示罗勒多糖可能治疗特发性肺纤维化的机制。方法 A549细胞分为正常对照组、模型组(TGF-β5 ng·m L~(-1))、罗勒多糖组(TGF-β5 ng·m L~(-1)+罗勒多糖200μg·m L~(-1)),观察各组细胞形态学变化;实时荧光定量PCR(RT-q PCR)法检测各组Ⅰ型胶原蛋白(colⅠ)和上皮间质转化标志物表达;ELISA法检测各组细胞羟脯氨酸(HYP)浓度。结果与正常对照组比较,模型组细胞成纤维样变;与模型组比较,罗勒多糖组细胞维持上皮细胞形态。与正常对照组比较,模型组colⅠ基因表达明显上调(P<0.01),E-cadherin基因表达下调(P<0.01),Vimentin、α-SMA基因表达上调(P<0.05);与模型组相比,罗勒多糖组E-cadherin基因表达上调(P<0.05),Vimentin、α-SMA、colⅠ基因表达下调(P<0.05)。与正常对照组比较,模型组HYP含量增加(P<0.05);与模型组比较,罗勒多糖组HYP含量减少(P<0.05)。结论罗勒多糖能抑制TGF-β诱导的A549细胞上皮间质转化,其作用机制与下调colⅠ、Vimentin、α-SMA基因表达,上调E-cadherin基因表达,降低HYP含量有关,罗勒多糖可用于治疗特发性肺纤维化。
Objective To study the effect of basilain on inhibiting epithelial-mesenchymal transition of A549 cells induced by transforming growth factor-β (TGF-β) and to reveal the possible mechanism of basil in the treatment of idiopathic pulmonary fibrosis. Methods A549 cells were divided into normal control group, model group (TGF-β5 ng · m L -1), basilarm group (TGF-β 5 ng · m L -1) and basil 200μg · m L ~ (-1)). The morphological changes of cells in each group were observed. The expression of type Ⅰ collagen (Ⅰ) and epithelial-mesenchymal transition markers (TKIs) were detected by real-time fluorescence quantitative PCR Hydroxyproline (HYP) concentration. Results Compared with the normal control group, the cells in the model group were fibroblast-like. Compared with the model group, the basilar cells maintained epithelial morphology. Compared with the normal control group, the expression of col Ⅰ gene in model group was significantly increased (P <0.01), the expression of E-cadherin gene was down-regulated (P <0.01), and the expression of α-SMA and Vimentin was up-regulated (P <0.05). The expression of Vimentin, α-SMA, and colⅠwas down-regulated in basilain group (P <0.05). Compared with the normal control group, HYP content in the model group increased (P <0.05). Compared with the model group, HYP content in the basil group decreased (P <0.05). Conclusion Basil polysaccharide can inhibit epithelial-mesenchymal transition of A549 cells induced by TGF-β, and its mechanism may be related to down-regulation of gene expression of colⅠ, Vimentin and α-SMA, up-regulation of E-cadherin gene expression and decrease of HYP content. Pulmonary fibrosis.