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

作　　者：SAIFEI XIE HUI XIE JINCAI GUO JIN TAN YULIN YU MINYI ZHANG SHANG WEN 

机构地区：[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

出　　处：《BIOCELL》2024年第4期591-599,共9页生物细胞（英文）

基　　金：This work was supported by the National Natural Science Foundation of China(Nos.81874496,82374530);the Clinical Medical Technology Innovation Guide Project of Hunan Province(No.2020SK53206);the Natural Science Foundation of Hunan Province(No.2021JJ70062);the Changsha Natural Science Foundation Project(No.kq2014019);the Health Special Fund Research Project of Hunan Province(No.B2020-07);the Clinical Pharmaceutical Research Fund of Hunan Medical Association(No.B202012).

摘　　要：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 submucousfibrosis(OSF)treatment.Methods:Human oral mucosafibroblasts(hOMF)were induced with transforming growth factor beta1(TGF-β1)and intervened with Pue.Expressions offibrosis-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 betweenfibroblast 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 declinedfibrosis 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.

关 键 词：PUERARIN miR-30b-5p FAP Oral submucous fibrosis 

分 类 号：R78[医药卫生—口腔医学]