@Article{biocell.2024.046691,
AUTHOR = {SAIFEI XIE, HUI XIE, JINCAI GUO, JIN TAN, YULIN YU, MINYI ZHANG, SHANG WEN},
TITLE = {Puerarin mediated miR-30b-5p targeting fibroblast activation protein against oral submucous fibrosis},
JOURNAL = {BIOCELL},
VOLUME = {48},
YEAR = {2024},
NUMBER = {4},
PAGES = {591--599},
URL = {http://www.techscience.com/biocell/v48n4/56128},
ISSN = {1667-5746},
ABSTRACT = { <b>Background:</b> Puerarin (Pue) has been reported to be a natural active ingredient with multiple antifibrotic properties. This work aimed at exploring the function of Pue in oral submucous fibrosis (OSF) treatment. <b>Methods:</b> Human oral mucosa fibroblasts (hOMF) were induced with transforming growth factor beta1 (TGF-β1) and intervened with Pue. Expressions of fibrosis-related markers were analyzed by Western blot and IF staining. Cell viability was characterized by the CCK-8 assay. Expressions of miR-30 family members were quantified by qRT-PCR. The correlation between fibroblast activation protein (FAP) and miR-30 family expression was evaluated by the Pearson correlation coefficient. Bioinformatics prediction and dual-luciferase reporter assay were employed to verify the regulation between FAP and miR-30b-5p. The specific mechanism of Pue on OSF was explored through the promotion or inhibition of miR-30b-5p. <b>Results:</b> After induction by TGF-β1, hOMF showed upregulated Collagen I, Collagen III, and FAP expressions, while miR-30 family expression was downregulated with miR-30b-5p being the most significant. Pue intervention inhibited the excessive proliferation of TGF-β1-induced hOMF, downregulated FAP, collagen type 3 (COL3A1), collagen type 1 (COL1A1), matrix metalloproteinase 1 (MMP1), and matrix metalloproteinase 3 (MMP3) expressions, and restored miR-30 family expression. Bioinformatics prediction and dual-luciferase reporter assay revealed that miR-30b-5p selectively inhibited FAP expression. Mechanistically, miR-30b-5p mimic suppressed the excessive proliferation of TGF-β1-induced hOMF and declined fibrosis levels. Pue intervention significantly reversed the promotion of TGF-β1-induced OSF by miR-30b-5p inhibition. <b>Conclusion:</b> Pue mediated miR-30b-5p targeting FAP against OSF, which provided a theoretical basis for the pathogenesis research and Pue application in OSF.},
DOI = {10.32604/biocell.2024.046691}
}