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Mechanism of Fuzheng Quxie Prescription Against Liver Injury of ConA Model Mice / 中国实验方剂学杂志

Jun-hong LIU; Ping-sheng ZHU; Zheng-wang ZHU; Zhi-ying WANG.
Artículo en Zh | WPRIM | ID: wpr-801867

Objective:

To study the protective effect of Fuzheng Quxie prescription on liver injury by influencing the expressions of tumor necrosis factor (TNF)-α, apoptosis factor (Fas), apoptosis factor ligand (FasL), and macrophages (CD68) in the liver tissues of concanavalin A(ConA) model mice.

Method:

The sixty mice were randomly divided into normal group, model group,bicyclol group (62.5 mg·kg-1), and low, medium and high-dose Fuzheng Quxie prescription groups(50.3,67.0,83.8 g·kg-1). The normal group and the model group were given the equal volume of pure water for 7 d. They were fasted for 12 hours before the last administration. At 2nd hour after the last administration, phosphate buffer(PBS) was injected into the caudal vein of the normal group, and ConA (20 mg·kg-1) was injected into the caudal vein of the other groups for modeling. The animals were put to death six hours later after the injection, and the expressions of TNF-α, Fas, FasL and CD68 in liver tissues were observed by immunohistochemistry.

Result:

Compared with normal group, the expressions of TNF-α, Fas, FasL and CD68 in the liver tissues of the model group were significantly increased(Pα, FasL and CD68 in liver tissues of the bicyclol group were significantly decreased compared with the model group(Pα, FasL and CD68 in liver tissues were significantly decreased in medium and high-dose Fuzheng Quxie prescription groups (PP

Conclusion:

Fuzheng Quxie prescription can effectively reduce the apoptosis of liver cells in ConA model mice by inhibiting Kupffer cells and Fas/FasL system activation.
Biblioteca responsable: WPRO