Validation and functional analysis of the critical proteins in combination with taurine, epigallocatechin gallate and genistein against liver fibrosis in rats

In our previous works, we highlight nine candidates (Cathepsin D, Lamp1, Tpi1, Fgb, FVII, Mst4, CDK4, Hdgf and Glud1) that might be key proteins of combination therapy anti-fibrosis in rats. In this research, in order to verify the function of candidates, gene or protein expression of the nine candi...

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Published in:	Biomedicine & pharmacotherapy 2019-07, Vol.115, p.108975-108975, Article 108975
Main Authors:	Luo, Ying, Huo, Yani, Song, Pengshu, Zhang, Xuerong, Liao, Ming
Format:	Article
Language:	eng
Subjects:	Animals Catechin - administration & dosage Catechin - analogs & derivatives Catechin - therapeutic use Cell Line Cell Proliferation - drug effects Combination therapy Drug Therapy, Combination Factor VII - metabolism Genistein - administration & dosage Genistein - therapeutic use Hepatic stellate cell Hepatic Stellate Cells - drug effects Hepatic Stellate Cells - metabolism Hepatic Stellate Cells - pathology Key proteins Liver - drug effects Liver - metabolism Liver - pathology Liver Cirrhosis, Experimental - drug therapy Liver Cirrhosis, Experimental - metabolism Liver Cirrhosis, Experimental - pathology Liver fibrosis Liver Function Tests Rats, Sprague-Dawley Taurine - administration & dosage Taurine - therapeutic use
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Summary:	In our previous works, we highlight nine candidates (Cathepsin D, Lamp1, Tpi1, Fgb, FVII, Mst4, CDK4, Hdgf and Glud1) that might be key proteins of combination therapy anti-fibrosis in rats. In this research, in order to verify the function of candidates, gene or protein expression of the nine candidates was verified by Western blot and RT-qPCR, and enzyme-linked immunosorbent assay in vitro and vivo. The expression of Fgb, Tpi1, CDK4, Mst4 and FVII significantly changed and matched with previous results after combination treating fibrosis rats or hepatic stellate cells (HSCs). These proteins may play crucial roles in anti-fibrosis. In particular, FVII take on pivotal role in combination therapy against liver fibrosis. The viability and cycle of HSCs was determined using CCK8 assay and Flow Cytometry, respectively. The results indicate that an overexpression of FVII could accelerate HSC proliferation and reduce the pharmacologic sensitivity. Combination therapy may inhibit HSC proliferation by blocking cell cycle in S phase. Although further studies are necessary to determine the precise protein functions, this research provides the possible molecular mechanisms and signaling pathways of combination therapy against liver fibrosis.
ISSN:	0753-3322 1950-6007