Open Access

ARTICLE

Puerarin mediated miR-30b-5p targeting fibroblast activation protein against oral submucous fibrosis

SAIFEI XIE^1,2,4, HUI XIE^2,*, JINCAI GUO³, JIN TAN⁴, YULIN YU¹, MINYI ZHANG¹, SHANG WEN¹

1 Department of Periodontal Mucosa, Hunan University of Chinese Medicine, Changsha, China
2 Department of Periodontal Mucosa, Changsha Stomatology Hospital, Changsha, China
3 Department of Pharmacy, Changsha Stomatology Hospital, Changsha, China
4 Department of Stomatology, The First Hospital of Hunan University of Chinese Medicine, Changsha, China

* Corresponding Author: HUI XIE. Email:

BIOCELL 2024, 48(4), 591-599. https://doi.org/10.32604/biocell.2024.046691

Received 11 October 2023; Accepted 11 December 2023; Issue published 09 April 2024

Abstract

Background: 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. Methods: 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. Results: 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. Conclusion: Pue mediated miR-30b-5p targeting FAP against OSF, which provided a theoretical basis for the pathogenesis research and Pue application in OSF.

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