Molecular Mechanism of White Tea Extract Regulating EMT in Type &#x02161; Alveolar Cells via miR-146a to Inhibit Pulmonary Fibrosis in Sj&#x000f6;gren&#x02019;s Syndrome

ZHANG Jingjing; ZHU Yuelan; WANG Chao

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Journal of Tea Science ›› 2026, Vol. 46 ›› Issue (3) : 535-544.

Molecular Mechanism of White Tea Extract Regulating EMT in Type Ⅱ Alveolar Cells via miR-146a to Inhibit Pulmonary Fibrosis in Sjögren’s Syndrome

ZHANG Jingjing, ZHU Yuelan, WANG Chao^*

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Abstract

This paper aimed to investigate the mechanism of white tea extract on type Ⅱ alveolar cells and the expression level of microRNA-146a (miR-146a) in Sjogren’s syndrome complicated with pulmonary fibrosis. Human alveolar epithelial A549 cells were divided into different groups: the blank group was not treated with transforming growth factor-β1 (TGF-β1), the TGF-β1-induced group was treated with TGF-β1 without any intervention, the white tea extract group was treated with 50 μg·mL^-1 white tea extract after TGF-β1 induction, the miR-146a mimic group was transfected with 6 μL miR-146a mimic after TGF-β1 induction; and the white tea extract + miR-146a mimic group was intervened with 50 μg·mL^-1 white tea extract combined with 6 μL miR-146a mimic after TGF-β1 induction. Cell morphology was observed under a microscope and cell viability was detected by CCK-8 assay. The fluorescence intensities of E-cadherin and α-SMA proteins were measured by immunofluorescence. The expressions of SP-C and PDGFRα were detected by Western blotting. The expression levels of miR-146a, TGF-β1 and Smad2 were determined by qRT-PCR. The results show that compared with the blank group, the TGF-β1-induced group exhibited increased cell viability, fluorescence intensity of α-SMA protein, increased expressions of SP-C, PDGFRα and TGF-β1, as well as decreased expressions of E-cadherin and miR-146a (P<0.05). Compared with the TGF-β1-induced group, the white tea extract group and the miR-146a mimic group showed decreased cell viability, fluorescence intensity of α-SMA, expressions of SP-C, PDGFRα and TGF-β1, together with increased expressions of E-cadherin and miR-146a (P<0.05), with no statistically significant difference between the two groups (P>0.05). Compared with the miR-146a mimic group, the aforementioned indicators in the white tea extract + miR-146a mimic group changed more significantly (P<0.05). This study indicates that white tea extract can markedly inhibit the abnormal activation of A549 cells induced by TGF-β1, reverse the process of epithelial-mesenchymal transition (EMT) and downregulate fibroblast-related activity indicators. Its mechanism may be related to the up-regulation of miR-146a expression and the regulation of the TGF-β1/Smad2 signaling pathway.

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Sjögren’s syndrome with pulmonary fibrosis / white tea extract / type Ⅱ alveolar cells / TGF-β1

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ZHANG Jingjing, ZHU Yuelan, WANG Chao. Molecular Mechanism of White Tea Extract Regulating EMT in Type Ⅱ Alveolar Cells via miR-146a to Inhibit Pulmonary Fibrosis in Sjögren’s Syndrome[J]. Journal of Tea Science. 2026, 46(3): 535-544

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