栝楼薤白半夏汤预处理对大鼠心肌缺血再灌注损伤 JAK-STAT细胞信号传导调节的研究

段雪涛; 晋红宾; 易亚乔; 张炳填

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栝楼薤白半夏汤预处理对大鼠心肌缺血再灌注损伤 JAK-STAT细胞信号传导调节的研究

更新时间：2024-01-04

- 栝楼薤白半夏汤预处理对大鼠心肌缺血再灌注损伤 JAK-STAT细胞信号传导调节的研究
- JAK-STAT Cell Signaling Pathways Adjusting by Gualou Xiebai Banxia Decoction Preconditioning in Myocardial Ischemia Reperfusion Injury
- 中国实验方剂学杂志 2011年17卷第24期页码：147-150
- 作者机构：
- 作者简介：
- 基金信息：
  
  湖南省教育厅重点项目(06A053);湖南省自然科学基金(07JJ6049);湖南省教育厅资助一般项目(09C722)
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- 纸质出版日期：2011
- 稿件说明：
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段雪涛, 晋红宾, 易亚乔, 等. 栝楼薤白半夏汤预处理对大鼠心肌缺血再灌注损伤 JAK-STAT细胞信号传导调节的研究[J]. 中国实验方剂学杂志, 2011,17(24):147-150.

DUAN Xue-tao, JIN Hong-bin, YI Ya-qiao, et al. JAK-STAT Cell Signaling Pathways Adjusting by Gualou Xiebai Banxia Decoction Preconditioning in Myocardial Ischemia Reperfusion Injury[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(24): 147-150.
段雪涛, 晋红宾, 易亚乔, 等. 栝楼薤白半夏汤预处理对大鼠心肌缺血再灌注损伤 JAK-STAT细胞信号传导调节的研究[J]. 中国实验方剂学杂志, 2011,17(24):147-150. DOI：

DUAN Xue-tao, JIN Hong-bin, YI Ya-qiao, et al. JAK-STAT Cell Signaling Pathways Adjusting by Gualou Xiebai Banxia Decoction Preconditioning in Myocardial Ischemia Reperfusion Injury[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(24): 147-150. DOI：

摘要

目的 :探讨栝楼薤白半夏汤(GXBD)对大鼠心肌缺血再灌注损伤Janus激酶信号转导子与转录激活子(JAK-STAT)细胞信号传导的调节作用。方法 :将60只雄性SD大鼠随机分为空白对照(A)组

缺血再灌注(B)组(I/R)

缺血预处理(C)组(IPC)

GXBD预处理(D)组

AG490处理(E)组

每组8只。结扎大鼠左冠状动脉前降支30 min

再灌注90 min制作心肌缺血再灌注损伤模型。A

E组每天ig 1次

连续3 d

末次ig后1 h行冠脉结扎。A

B组给等容量生理盐水

E组分别以4.95 g·kg-1 ig给药

E组AG 490以2 mg·kg-1剂量于造模前1 h舌下静脉注射

造模结束后

分别测定各组血清腺苷(Ado)和缓激肽(BK)水平

心肌梗死面积及心肌组织JAK2

STAT3的蛋白表达。结果 :模型组和AG490组血清Ado和BK水平显著下降(P<0.05)

心肌梗死面积显著扩大(P<0.01)

JAK2

STAT3蛋白表达显著减少(P<0.05);GXBD组和IPC组均可使Ado

JAK2

STAT3水平显著升高(P<0.05)

心肌梗死面积显著缩小(P<0.01)。结论 :GXBD能通过JAK-STAT细胞信号传导通路的介导

上调JAK2

STAT3的蛋白表达

升高Ado

BK含量

减少心肌梗死面积

对缺血再灌注心肌起保护作用。

Abstract

Objective : To explore JAK-STAT cell signaling pathways adjusting by Gualou Xiebai Banxia decoction precinditioning in myocardial ischemia reperfusion injury. Method :Sixty male SD rats were randomly divided into blank control (A) group

ischemia /reperfusion (B) group (I/R)

ischemia preconditioning (C) group (IPC)

GXBD pretreatment (D) group

AG490 processing (E) groups

there were 8 rats in each group. Ligation of the left anterior descending coronary artery for 30 minutes and 90 minutes reperfusion was performed

to make myocardial ischemia reperfusion injury

group were were given physiological saline

group D and E were treated with 4.95 g·kg-1 doses of GXBD and 2 mg·kg-1 dose of AG490.before 1 h of modelling. The serum adenosine (Ado) and gentle shock peptide (BK) level were measured

myocardial infarction area and JAK2

STAT3 protein expression of the myocardial tissue were detected. Result : The serum Ado and BK level in the model group and AG490 group were significantly decreased (P<0.05)

myocardial infarction area expanded significantly (P<0.01)

JAK2

STAT3 protein expression significantly reduced (P<0.05); GXBD group and the IPC group could make Ado

JAK2

STAT3 level significantly increased (P<0.05)

myocardial infarction area reduced significantly (P<0.01). Conclusion: GXBD can raise the protein expressionof JAK2

STAT3

Adoand BK level and reduce myocardial infarction area to protect ischemia-reperfusion myocardial injury.

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