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Sulforaphane inhibits the activation of hepatic stellate cell by miRNA-423-5p targeting suppressor of fused.
- Source :
-
Human cell [Hum Cell] 2019 Oct; Vol. 32 (4), pp. 403-410. Date of Electronic Publication: 2019 Jul 05. - Publication Year :
- 2019
-
Abstract
- Liver fibrosis, a common pathological process in chronic liver diseases, is characterized by excessive accumulation of extracellular matrix proteins and considered as a wound healing response to chronic liver injury. Hepatic stellate cell (HSC) activation plays a key role in liver fibrosis development. Previous studies showed that sulforaphane (SFN) has wide protective effects against tissue injury and inflammation. Accumulating evidence has shown that microRNAs play important roles in the development of hepatic fibrosis, some of which have been identified as potential therapeutic targets. This study was conducted to explore the role of SFN in the suppression of HSC activation. Quantitative real-time PCR showed that HSC miR-423-5p levels were up-regulated during HSC activation and down-regulated after SFN administration. Further, transfection of a miR-423-5p mimic demonstrated that inhibition of HSC activation by SFN required down-regulation of miR-423-5p. We showed that suppressor of fused is the direct target of miR-423-5p. SFN may play a role in inhibiting hepatic fibrosis by downregulating miRNA-423-5p. MiRNA-423-5p may be useful as a therapeutic target for treating hepatic fibrosis.
- Subjects :
- Cell Line
Depression, Chemical
Down-Regulation drug effects
Humans
Isothiocyanates therapeutic use
Liver Cirrhosis drug therapy
MicroRNAs genetics
Molecular Targeted Therapy
Sulfoxides
Cell Survival drug effects
Cell Survival genetics
Hepatic Stellate Cells physiology
Isothiocyanates pharmacology
Liver Cirrhosis etiology
Liver Cirrhosis genetics
MicroRNAs metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1749-0774
- Volume :
- 32
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Human cell
- Publication Type :
- Academic Journal
- Accession number :
- 31278688
- Full Text :
- https://doi.org/10.1007/s13577-019-00264-2