Interferon alpha-2a and apoptosis of hepatic stellate cells in rats with hepatic fibrosis

doi:10.3969/j.issn.2095-4344.2013.11.013

Abstract

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 stellate 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 equally 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, 12×10⁴U/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 collected 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 stellate cells.
RESULTS AND CONCLUSION: Pathological morphology of the liver tissue demonstrated that the hepatic fibrosis model was successfully 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, especially in the 12×10⁴U/kg interferon alpha 2a intervention group as compared the model group. In addition, there was no expression of a-smooth muscle actin in the 6×10⁴U/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 stellate cells, and this regulatory role is possibly related to interferon alpha 2a dose.

Key words: tissue construction, tissue construction and bioactive factor, hepatic fibrosis, liver, interferon alpha-2a, Bcl-2, Bax, hepatic stellate cells, cell apoptosis, provincial grants-supported paper, tissue construction photographs-containing paper

CLC Number:

R318

Liu Cui-yun, Zhang Wei, Liu Pei-pei, Ye Chang-gen, Yi Zhen, Sun Shui-lin. Interferon alpha-2a and apoptosis of hepatic stellate cells in rats with hepatic fibrosis[J]. Chinese Journal of Tissue Engineering Research, 2013, 17(11): 1987-1992.

Figures/Tables 5

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