中国组织工程研究Issue(11)：1987-1992,6.DOI:10.3969/j.issn.2095-4344.2013.11.013
干扰素α-2a与肝纤维化大鼠肝星状细胞的凋亡*★
Interferon alpha-2a and apoptosis of hepatic stellate cells in rats with hepatic fibrosis
摘要
Abstract
BACKGROUND: Up to now, the mechanism underlying interferon alpha 2a to improve hepatic fibrosis has not been clarified. OBJECTIVE: To investigate the effect of interferon alpha 2a on hepatic stel ate cells apoptosis in the CCl4-induced hepatic fibrosis rat model. METHODS: We established the CCl4-induced hepatic fibrosis models in rats. Fifty healthy female Sprague-Dawley rats were equal y and randomly divided into five groups, certainly each group included 10. Five groups were saline control group, hepatic fibrosis model group (model group), 6×104 U/kg interferon alpha 2a intervention group, 12×104 U/kg interferon alpha 2a intervention group and 6×104 U/kg interferon alpha 2a control group. At 8 weeks after modeling, blood and liver tissues were col ected to detect the indicators of hepatic fibrosis; the expression of bcl-2 and bax in the liver tissue was analyzed with semi-quantitative reverse transcription-PCR; and immunohistochemical staining was used to mark a-smooth muscle actin in activated hepatic stel ate cells. RESULTS AND CONCLUSION: Pathological morphology of the liver tissue demonstrated that the hepatic fibrosis model was successful y established. The model group had fibrosis significantly around the portal area; in addition, Mans-like fibers and fibrous septa formed. Different interferon alpha 2a intervention groups had fibrosis relief to different extent. a-smooth muscle actin had a great amount of positive expression in the model group, while the positive expression of a-smooth muscle actin was lower in the interferon alpha 2a intervention groups, especial y in the 12×104 U/kg interferon alpha 2a intervention group as compared the model group. In addition, there was no expression of a-smooth muscle actin in the 6×104 U/kg interferon alpha 2a control group. Interferon alpha 2a could down-regulate bcl-2 expression and up-regulate bax expression in CCl4-induced hepatic fibrosis models. These findings indicate that the mechanism of interferon alpha 2a blocking CCl4-induced hepatic fibrosis is mainly present by regulating the expression of bcl-2 and bax to induce apoptosis of hepatic stel ate cells, and this regulatory role is possibly related to interferon alpha 2a dose.关键词
组织构建/组织构建与生物活性因子/肝纤维化/肝/干扰素 α-2a/Bcl-2/Bax/肝星状细胞/细胞凋亡/省级基金/组织构建图片文章Key words
tissue construction/tissue construction and bioactive factor/hepatic fibrosis/liver/interferon alpha-2a/Bcl-2/Bax/hepatic stel ate cells/cel apoptosis/provincial grants-supported paper/tissue construction photographs-containing paper分类
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刘翠芸,张伟,刘佩佩,叶长根,易珍,孙水林..干扰素α-2a与肝纤维化大鼠肝星状细胞的凋亡*★[J].中国组织工程研究,2013,(11):1987-1992,6.基金项目
江西省科技厅基金资助项目(2009BSB11115)。Supported by：the Fund from the Science and Technology Bureau of Jiangxi Province, No.2009BSB11115* （2009BSB11115）
