Combined Taurine, Epigallocatechin Gallate and Genistein Therapy Reduces HSC-T6 Cell Proliferation and Modulates the Expression of Fibrogenic Factors

Li, Yan; Luo, Ying; Zhang, Xuerong; Lin, Xiaobo; He, Miao; Liao, Ming

doi:10.3390/ijms141020543

Cited by 21 publications

(11 citation statements)

References 34 publications

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“…During hepatic fibrogenesis, collagen deposition (primarily collagen types I and III) accounts for 50% of the total proteins in the fibrotic liver (Li et al, ). Therefore, we found the level of col‐1 was effectively reduced by amirolide in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of ASICs reduces rat hepatic stellate cells activity and liver fibrosis: An in vitro and in vivo study

Pan

Wu²,

Wang³

et al. 2014

Cell Biology International

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Hepatic fibrosis is a chronic inflammation-associated disease, which is involved in the infiltration of inflammatory cells and releasing of proinflammatory cytokines. In the pathological process, protons are released by damaged cells and acidosis is considered to play a critical role in cell injury. Although the underlying mechanism (s) remain ill-defined, ASICs (acid-sensing ion channels) are assumed to be involved in this process. The diuretic, amiloride, is neuroprotective in models of cerebral ischemia, a property attributable to the inhibition of central ASICs by the drug. However, the effect of inhibition of ASICs by amiloride in the liver fibrotic process remains unclear. We found that amiloride (25, 50, or 100 μM) could restrain acid-induced HSCs at pH6 in vitro. In vivo experiments showed that amiloride could significantly alleviate liver injury, decreasing levels of profibrogenic cytokines, collagen deposition, and reducing pathological tissue damage. In summary, amiloride inhibits hepatic fibrosis in vivo and in vitro, which is probably associated with the downregulation of ASICs.

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Section: Discussionmentioning

confidence: 99%

Inhibition of ASICs reduces rat hepatic stellate cells activity and liver fibrosis: An in vitro and in vivo study

Pan

Wu²,

Wang³

et al. 2014

Cell Biology International

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“…Moreover, the MTT result showed that the activity of HSCs was increased under acidic conditions. A previous study indicated that collagen deposition mainly accounts for proteins in fibrotic liver [29]; thus, we can say that the inhibition of ASIC1a may relieve acid‐induced activated HSC activity. Our results also showed that the ASIC1a expression plasmid group aggravated the acid‐induced cell activation.…”

Section: Discussionmentioning

confidence: 82%

ASIC1a inhibits cell pyroptosis induced by acid‐induced activation of rat hepatic stellate cells

Kong

Huang

et al. 2020

FEBS Open Bio

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The activation of hepatic stellate cells (HSCs) is associated with liver fibrosis, the pathological feature of most forms of chronic hepatic damage, and is accompanied by abnormal deposition of the extracellular matrix (ECM). During the pathological process, acid‐sensing ion channel 1a (ASIC1a), which is responsible for Ca2+ transportation, is involved in the activation of HSCs. It has previously been identified that ASIC1a is related to pyroptosis in articular chondrocytes. However, it remains unclear whether ASIC1a restrains pyroptosis during liver fibrosis. Here, we determined that the levels of pyroptosis‐associated speck‐like protein, gasdermin D, caspase‐1, nucleotide‐binding oligomerization domain (NOD)‐like receptor 3, and apoptosis‐associated speck‐like protein (ASC) decreased, while the level of α‐smooth muscle actin and collagen‐I increased upon introduction of ASIC1a into an acid‐induced model. Inhibition or silencing of ASIC1a and the use of Ca2+‐free medium were able to promote the pyroptosis of activated HSCs, which reduced their deposition. In summary, our study indicates that ASIC1a inhibits pyroptosis of HSCs and that inhibition of ASIC1a may be able to promote pyroptosis to relieve liver fibrosis.

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“…A variety of biological factors are involved in the pathogenesis of liver fibrosis. As an approach to investigate the multiple signaling pathways that may contribute to liver fibrosis, our group previously reported that combination therapy with taurine, EGCG and genistein exhibits a protective effect against liver fibrosis in vivo and in vitro ( 15 , 18 ). In the present study, the mechanistic underpinnings of this effect in HSC-T6 cells were evaluated using a proteomic approach.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, experimental analysis of HSC activation is an important aspect of research into the pathogenesis hepatic fibrosis. Our group previously reported that combination therapy with taurine, epigallocatechin gallate (EGCG) and genistein exhibits a protective effect against alcohol-induced liver fibrosis and also reduces cell proliferation and the expression of fibrogenic factors in the rat HSC-T6 cell line ( 15 , 18 ).…”

Section: Introductionmentioning

confidence: 99%

Anti‑fibrosis activity of combination therapy with epigallocatechin gallate, taurine and genistein by regulating glycolysis, gluconeogenesis, and ribosomal and lysosomal signaling pathways in HSC‑T6 cells

Zhu

Huo

et al. 2018

Exp Ther Med

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A previous study by our group indicated that combined treatment with taurine, epigallocatechin gallate (EGCG) and genistein protects against liver fibrosis. The aim of the present study was to elucidate the antifibrotic mechanism of this combination treatment using isobaric tag for relative and absolute quantification (iTRAQ)-based proteomics in an activated rat hepatic stellate cell (HSC) line. In the present study, HSC-T6 cells were incubated with taurine, EGCG and genistein, and cellular proteins were extracted and processed for iTRAQ labeling. Quantification and identification of proteins was performed using two-dimensional liquid chromatography coupled with tandem mass spectrometry. Proteomic analysis indicated that the expression of 166 proteins were significantly altered in response to combination treatment with taurine, EGCG and genistein. A total 76 of these proteins were upregulated and 90 were downregulated. Differentially expressed proteins were grouped according to their association with specific Kyoto Encyclopedia of Genes and Genomes pathways. The results indicated that the differentially expressed proteins hexokinase-2 and lysosome-associated membrane glycoprotein 1 were associated with glycolysis, gluconeogenesis and lysosome signaling pathways. The expression of these proteins was validated using western blot analysis; the expression of hexokinase-2 was significantly decreased and the expression of lysosome-associated membrane glycoprotein 1 was significantly increased in HSC-T6 cells treated with taurine, EGCG and genistein compared with the control, respectively (P<0.05). These results were in accordance with the changes in protein expression identified using the iTRAQ approach. Therefore, the antifibrotic effect of combined therapy with taurine, EGCG and genistein may be associated with the activation of several pathways in HSCs, including glycolysis, gluconeogenesis, and the ribosome and lysosome signaling pathways. The differentially expressed proteins identified in the current study may be useful for treatment of liver fibrosis in the future.

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Combined Taurine, Epigallocatechin Gallate and Genistein Therapy Reduces HSC-T6 Cell Proliferation and Modulates the Expression of Fibrogenic Factors

Cited by 21 publications

References 34 publications

Inhibition of ASICs reduces rat hepatic stellate cells activity and liver fibrosis: An in vitro and in vivo study

Inhibition of ASICs reduces rat hepatic stellate cells activity and liver fibrosis: An in vitro and in vivo study

ASIC1a inhibits cell pyroptosis induced by acid‐induced activation of rat hepatic stellate cells

Anti‑fibrosis activity of combination therapy with epigallocatechin gallate, taurine and genistein by regulating glycolysis, gluconeogenesis, and ribosomal and lysosomal signaling pathways in HSC‑T6 cells

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