Mechanism of Fuzheng Quxie Prescription Against Liver Injury of ConA Model Mice

Jun-hong LIU; Ping-sheng ZHU; Zheng-wang ZHU; Zhi-ying WANG

doi:10.13422/j.cnki.syfjx.20192040

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Mechanism of Fuzheng Quxie Prescription Against Liver Injury of ConA Model Mice

Pharmacology | 更新时间：2021-02-09

- Mechanism of Fuzheng Quxie Prescription Against Liver Injury of ConA Model Mice
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 20, Pages: 70-75(2019)
- 作者机构：
  
  河南中医药大学，郑州　 450046
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20192040
  CLC： R2-0; R285.5; R289
- Received：02 April 2019，
  
  Published Online：04 July 2019，
  
  Published：20 October 2019
- 稿件说明：
移动端阅览
Jun-hong LIU, Ping-sheng ZHU, Zheng-wang ZHU, et al. Mechanism of Fuzheng Quxie Prescription Against Liver Injury of ConA Model Mice[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(20): 70-75.
DOI：

Jun-hong LIU, Ping-sheng ZHU, Zheng-wang ZHU, et al. Mechanism of Fuzheng Quxie Prescription Against Liver Injury of ConA Model Mice[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(20): 70-75. DOI： 10.13422/j.cnki.syfjx.20192040.

摘要

目的：

探讨扶正祛邪方通过对刀豆蛋白A(ConA)模型小鼠肝组织中肿瘤坏死因子-

(TNF-

)，凋亡因子(Fas)，凋亡因子配体(FasL)，巨噬细胞(CD68)表达的影响从而发挥对肝损伤的保护作用。

方法：

将60只小鼠随机分为正常组、模型组、双环醇组(62.5 mg·kg

－1

)、扶正祛邪方低、中、高剂量组(50.3，67.0，83.8 g·kg

－1

)。正常组和模型组给予等体积纯水，连续7 d。末次给药前禁食12 h，给药2 h后，正常组尾静脉注射磷酸盐缓冲液(PBS)，其余各组尾静脉注射ConA(20 mg·kg

－1

)造模。注射6 h后取材，免疫组化观测肝组织中TNF-

，FasL，CD68表达情况。

结果：

与正常组比较，模型组肝组织中TNF-

，Fas，FasL，CD68表达均显著升高(

0.01)，说明肝损伤模型复制成功；与模型组比较，双环醇组肝组织中TNF-

，FasL，CD68表达均显著降低(

0.01)；扶正祛邪方中、高剂量组肝组织中TNF-

，Fas，FasL，CD68表达均显著降低(

0.05，

0.01)。

结论：

扶正祛邪方可通过抑制Kupffer细胞和Fas/FasL系统的活化，有效减少ConA模型小鼠肝细胞凋亡。

Abstract

Objective:

To study the protective effect of Fuzheng Quxie prescription on liver injury by influencing the expressions of tumor necrosis factor (TNF)-

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 2

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-

Fas

FasL and CD68 in liver tissues were observed by immunohistochemistry.

Result:

Compared with normal group

the expressions of TNF-

Fas

FasL and CD68 in the liver tissues of the model group were significantly increased(

0.01)

indicating the successful replication of the liver injury model. The expressions of TNF-

FasL and CD68 in liver tissues of the bicyclol group were significantly decreased compared with the model group(

0.01). The expressions of TNF-

FasL and CD68 in liver tissues were significantly decreased in medium and high-dose Fuzheng Quxie prescription groups (

0.05

0.01).

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.

关键词

Keywords

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