Mangiferin Attenuates Prostatic Fibrosis in Benign Prostate Hyperplasia by Regulating miRNA-483-3p
10.3870/j.issn.1004-0781.2024.04.003
- VernacularTitle:芒果苷通过调节miRNA-483-3p减轻良性前列腺增生腺体纤维化
- Author:
Chuhao YANG
1
;
Jinglou CHEN
;
Tao CHEN
Author Information
1. 江汉大学附属医院药剂科,武汉 430014
- Keywords:
Mangiferin;
MicroRNA-483-3p;
Prostate;
Fibrosis
- From:
Herald of Medicine
2024;43(4):489-494
- CountryChina
- Language:Chinese
-
Abstract:
Objective This study was to investigate the ameliorative effects of mangiferin on prostatic fibrosis in benign prostatic hyperplasia(BPH)and the mechanism of action of regulating microRNA(miRNA)-483-3p.Methods The male mice were randomly divided into five groups:normal control group,BPH model control group,finasteride group,mangiferin group,and mangiferin+miRNA-483-3p antagonist group.The mice model of BPH was induced by castration and subcutaneous injection of tes-tosterone propionate.After 30 days,the prostatic collagen deposition was observed by masson and sirius red stain,and the level of hydroxyproline was detected.Prostatic mRNA levels of transforming grouth factor-β1(TGF-β1),mitogen-activated protein kinase 2(MK2),and mitogen-activated protein kinase kinase 6(MKK6),as well as the level of miRNA-483-3p,were detected by quantita-tive real-time PCR.Prostatic protein levels of TGF-β1,MK2,phosphorylated MK2(p-MK2),MKK6,and p-MKK6 were detected by western blotting.Finally,the binding effect of miRNA-483-3p on MK2 was evaluated by luciferase assay.Results Compared to normal control group,the prostatic collagen deposition,mRNA levels of TGF-β1,MK2,and MKK6,as well as protein levels of TGF-β1,p-MK2,and p-MKK6 were significantly increased(P<0.01),while the miRNA-483-3p level was significantly decreased in BPH model control group(P<0.01).Compared with BPH model control group,the mangiferin group was able to up-regulate the level of miRNA-483-3p,reduce the mRNA levels of TGF-β1,MK2,and MKK6,as well as the protein levels of TGF-β1,p-MK2,and p-MKK6,and alleviate prostatic collagen deposition.When compared to the mangiferin group,mangiferin+miRNA-483-3p antagomir significantly decreased the miRNA-483-3p level,increased the prostatic collagen deposition,mRNA levels of TGF-β1,MK2,and MKK6,as well as protein levels of TGF-β1,p-MK2,and p-MKK6(P<0.01).Luciferase assay showed that miRNA-483-3p could tar-get binding with MK2.Conclusion Mangiferin can attenuate prostatic fibrosis by regulating miRNA-483-3p and inhibiting MK2.