Limits...
Combined taurine, epigallocatechin gallate and genistein therapy reduces HSC-T6 cell proliferation and modulates the expression of fibrogenic factors.

Li Y, Luo Y, Zhang X, Lin X, He M, Liao M - Int J Mol Sci (2013)

Bottom Line: Combined drug treatment significantly inhibited cell proliferation and TGF-β1, Col-I, TIMP-1 and TIMP-2 mRNA expression in activated HSC-T6 cells, while the expression of MMP-2 mRNA increased.In conclusion, combined drug treatment with taurine, epigallocatechin gallate and genistein can inhibit HSC proliferation, and impact fibrosis-related gene and protein expression.The antifibrotic effects of this drug combination may be due to its effects on the expression of fibrogenic genes.

View Article: PubMed Central - PubMed

Affiliation: Guangxi University Library, Guangxi University, Nanning 530004, Guangxi, China. lminggx@163.com.

ABSTRACT
Hepatic fibrogenesis involves the activation of hepatic stellate cells (HSCs), which synthesize excess extracellular matrix and contribute to the development of liver fibrosis. In a prior study we tested the effect of combined treatment with taurine, epigallocatechin gallate and genistein on the development of alcohol-induced liver fibrosis in vitro. In this study, the biological activity of the combination of these molecules was assessed by measuring its effect on cell proliferation, fibrosis-related gene expression, and proteomic expression profiling in the activated HSC cell line, HSC-T6. HSC-T6 cells were incubated with different concentrations of the drug combination taurine, epigallocatechin gallate and genistein. Cell proliferation was evaluated by MTT assay. Transforming growth factor β1 (TGF-β1), collagen type I (Col-I), matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinases 1 and 2 (TIMP-1 and TIMP-2) mRNA were analyzed by semi-quantitative reverse-transcription PCR. Proteomic profiling of HSC-T6 cells was also performed by SELDI-TOF-MS. Combined drug treatment significantly inhibited cell proliferation and TGF-β1, Col-I, TIMP-1 and TIMP-2 mRNA expression in activated HSC-T6 cells, while the expression of MMP-2 mRNA increased. A total of 176 protein m/z peaks were identified. The intensities of 10 protein peaks were downregulated and two protein peaks were upregulated in HSC-T6 cells after combined drug treatment. In conclusion, combined drug treatment with taurine, epigallocatechin gallate and genistein can inhibit HSC proliferation, and impact fibrosis-related gene and protein expression. The antifibrotic effects of this drug combination may be due to its effects on the expression of fibrogenic genes.

Show MeSH

Related in: MedlinePlus

Proteomic analysis of HSC-T6 cells treated with a combination of taurine, EGCG and genistein. We performed a proteomic analysis of taurine, EGCG and genistein-treated HSC-T6 cells (A) and control HSC-T6 cells (B). Representative protein peaks and gel views of the peaks which positively correlated with fibrosis with a m/z 5798.33, 6735.19 and 6896.73 are shown.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3821629&req=5

f3-ijms-14-20543: Proteomic analysis of HSC-T6 cells treated with a combination of taurine, EGCG and genistein. We performed a proteomic analysis of taurine, EGCG and genistein-treated HSC-T6 cells (A) and control HSC-T6 cells (B). Representative protein peaks and gel views of the peaks which positively correlated with fibrosis with a m/z 5798.33, 6735.19 and 6896.73 are shown.

Mentions: In order to detect fibrosis-associated proteins in treated HSC-T6 cells, their proteome was analyzed by SELDI-TOF-MS. Note, for this analysis we only compared the cells in group I and group III. A total of 176 proteomic peaks were generated, 12 of these peaks had mean intensity values that differed significantly between control and treated cells. Ten protein peaks were lower in the treated cells and had mass-to-charge (m/z) ratios of 2897.76, 5361.62, 5562.06, 5645.97, 5798.33, 6141.22, 6499.74, 6623.38, 6735.19 and 6896.73. Two protein peaks, with a m/z of 4656.91 and 5078.35, were higher in treated cells (Table 1 and Figure 3).


Combined taurine, epigallocatechin gallate and genistein therapy reduces HSC-T6 cell proliferation and modulates the expression of fibrogenic factors.

Li Y, Luo Y, Zhang X, Lin X, He M, Liao M - Int J Mol Sci (2013)

Proteomic analysis of HSC-T6 cells treated with a combination of taurine, EGCG and genistein. We performed a proteomic analysis of taurine, EGCG and genistein-treated HSC-T6 cells (A) and control HSC-T6 cells (B). Representative protein peaks and gel views of the peaks which positively correlated with fibrosis with a m/z 5798.33, 6735.19 and 6896.73 are shown.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3821629&req=5

f3-ijms-14-20543: Proteomic analysis of HSC-T6 cells treated with a combination of taurine, EGCG and genistein. We performed a proteomic analysis of taurine, EGCG and genistein-treated HSC-T6 cells (A) and control HSC-T6 cells (B). Representative protein peaks and gel views of the peaks which positively correlated with fibrosis with a m/z 5798.33, 6735.19 and 6896.73 are shown.
Mentions: In order to detect fibrosis-associated proteins in treated HSC-T6 cells, their proteome was analyzed by SELDI-TOF-MS. Note, for this analysis we only compared the cells in group I and group III. A total of 176 proteomic peaks were generated, 12 of these peaks had mean intensity values that differed significantly between control and treated cells. Ten protein peaks were lower in the treated cells and had mass-to-charge (m/z) ratios of 2897.76, 5361.62, 5562.06, 5645.97, 5798.33, 6141.22, 6499.74, 6623.38, 6735.19 and 6896.73. Two protein peaks, with a m/z of 4656.91 and 5078.35, were higher in treated cells (Table 1 and Figure 3).

Bottom Line: Combined drug treatment significantly inhibited cell proliferation and TGF-β1, Col-I, TIMP-1 and TIMP-2 mRNA expression in activated HSC-T6 cells, while the expression of MMP-2 mRNA increased.In conclusion, combined drug treatment with taurine, epigallocatechin gallate and genistein can inhibit HSC proliferation, and impact fibrosis-related gene and protein expression.The antifibrotic effects of this drug combination may be due to its effects on the expression of fibrogenic genes.

View Article: PubMed Central - PubMed

Affiliation: Guangxi University Library, Guangxi University, Nanning 530004, Guangxi, China. lminggx@163.com.

ABSTRACT
Hepatic fibrogenesis involves the activation of hepatic stellate cells (HSCs), which synthesize excess extracellular matrix and contribute to the development of liver fibrosis. In a prior study we tested the effect of combined treatment with taurine, epigallocatechin gallate and genistein on the development of alcohol-induced liver fibrosis in vitro. In this study, the biological activity of the combination of these molecules was assessed by measuring its effect on cell proliferation, fibrosis-related gene expression, and proteomic expression profiling in the activated HSC cell line, HSC-T6. HSC-T6 cells were incubated with different concentrations of the drug combination taurine, epigallocatechin gallate and genistein. Cell proliferation was evaluated by MTT assay. Transforming growth factor β1 (TGF-β1), collagen type I (Col-I), matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinases 1 and 2 (TIMP-1 and TIMP-2) mRNA were analyzed by semi-quantitative reverse-transcription PCR. Proteomic profiling of HSC-T6 cells was also performed by SELDI-TOF-MS. Combined drug treatment significantly inhibited cell proliferation and TGF-β1, Col-I, TIMP-1 and TIMP-2 mRNA expression in activated HSC-T6 cells, while the expression of MMP-2 mRNA increased. A total of 176 protein m/z peaks were identified. The intensities of 10 protein peaks were downregulated and two protein peaks were upregulated in HSC-T6 cells after combined drug treatment. In conclusion, combined drug treatment with taurine, epigallocatechin gallate and genistein can inhibit HSC proliferation, and impact fibrosis-related gene and protein expression. The antifibrotic effects of this drug combination may be due to its effects on the expression of fibrogenic genes.

Show MeSH
Related in: MedlinePlus