Expression of Transforming Growth Factor-β_1 of Hepatic Stellate Cells of Hepatic Fibrosis Rat after Interleukin-10 Intervention
Wang Xiaozhong
Abstract
Wang Xiaozhong
Abstract
Objective To investigate the expression of transforming growth factor-β-1(TGF-β-1) of hepatic stellate cells(HSC) of hepatic fibrosis rat after treatment with interleukin-(IL-10) and the antifibrogenic role of IL-10. Methods Hepatic fibrosis was induced by CCl-4. Sixty male Spraque-Dawly(SD) rats were randomly divided into three groups: normal control group(group N, 8 rats), hepatic fibrosis model group(group C, 28 rats) and IL-10 treated group(group I, 24 rats). At the beginning of the 7th and 11th week, rats in each group were routinely perfused with pronase E and type Ⅳ collagnase through portal vein catheter and the suspension obtained from the digested liver was centrifuged with 11% nycodenz density gradient to isolate HSC. RT-PCR was used to analyze TGF-β-1 mRNA. Immunocytochemistry was performed to detect protein expression in cultured HSC. Results Hepatic fibrosis was developed with the increase of the injection frequency of CCl-4 and HSC were successfully isolated. At the 7th week, TGF-β-1mRNA increased in group C compared to group N(P0.01), and significantly decreased after IL-10 intervention(P0.01). At the 11th week, TGF-β-1mRNA in intervention group was still lower than CCl-4group(P0.01). The hepatic fibrosis immunochemistry were paralleled with TGF-β-1 expression. Conclusion The expression of TGF-β-1 increased in the early stage of hepatic fibrosis but decreased by IL-10 intervention. IL-10 play an antifibrogenic role in suppressing TGF-β-1 expression.
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Objective To investigate the expression of transforming growth factor-β-1(TGF-β-1) of hepatic stellate cells(HSC) of hepatic fibrosis rat after treatment with interleukin-(IL-10) and the antifibrogenic role of IL-10. Methods Hepatic fibrosis was induced by CCl-4. Sixty male Spraque-Dawly(SD) rats were randomly divided into three groups: normal control group(group N, 8 rats), hepatic fibrosis model group(group C, 28 rats) and IL-10 treated group(group I, 24 rats). At the beginning of the 7th and 11th week, rats in each group were routinely perfused with pronase E and type Ⅳ collagnase through portal vein catheter and the suspension obtained from the digested liver was centrifuged with 11% nycodenz density gradient to isolate HSC. RT-PCR was used to analyze TGF-β-1 mRNA. Immunocytochemistry was performed to detect protein expression in cultured HSC. Results Hepatic fibrosis was developed with the increase of the injection frequency of CCl-4 and HSC were successfully isolated. At the 7th week, TGF-β-1mRNA increased in group C compared to group N(P0.01), and significantly decreased after IL-10 intervention(P0.01). At the 11th week, TGF-β-1mRNA in intervention group was still lower than CCl-4group(P0.01). The hepatic fibrosis immunochemistry were paralleled with TGF-β-1 expression. Conclusion The expression of TGF-β-1 increased in the early stage of hepatic fibrosis but decreased by IL-10 intervention. IL-10 play an antifibrogenic role in suppressing TGF-β-1 expression.
Key concepts: Hepatic stellate cell, Hepatic fibrosis, Immunochemistry, Internal medicine, Fibrosis, Transforming growth factor, Endocrinology, Medicine