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Cell Immunol:*新复方中药研究成果

来自华中科技大学同济医学院协和心内科、心血管病研究所的研究人员发布了题为“Qiliqiangxin regulates thebalance between tumor necrosis factor-alpha and interleukin-10 andimproves cardiac function in rats with myocardialinfarction”的研究成果,研究分析了芪苈强心调节急性心肌梗死大鼠心肌TNF2α和IL210表达,这一研究成果公布在《CellImmunol》杂志上。

参与研究的包括廖玉华教授等人,廖玉华教授现任华中科技大学同济医学院附属协和医院心内科主任,教授,主任医师,博士生导师,中华内科学会湖北分会副主任委员、中华心血管病学会武汉分会副主任委员、国际心血管病**学会委员。

 

 

芪苈强心胶囊是以岭药业研发**心力衰竭的中成药,临床试验证实芪苈强心胶囊具有强心、**、扩血管作用,**轻、中度充血性心力衰竭**有效。这是中国头个被国际权威杂志认可具有**调节、抑制心室重构作用的复方中药。

这项研究中,大鼠急性心肌梗死后给予芪苈强心**后,心功能比单纯心肌梗死组有所好转,左室射血分数上升,心肌收缩能力部分增强,尤其在持续给药4周后心功能改善效果更明显,相关性分析结果表明,心功能的改善可能与**调节心肌细胞分泌的TNF2α/IL210比例改变有关。

这一研究采用芪苈强心**AMI大鼠,结果发现:心肌梗死区浸润的**细胞计数在**组与梗死组无显著差异,即全身炎症反应招募的**反应无明显差别;而心肌梗死后健存心肌细胞表达的细胞因子**组与梗死组存在显著差异。心肌梗死后心肌细胞表达TNF2α、IL210等细胞因子,说明心肌细胞在病理状态下具有炎症因子自分泌作用,这些细胞因子参与AMI后炎症反应,当促炎因子高于**因子时,可导致心肌坏死后心室重塑,心功能下降。心肌梗死大鼠给予芪苈强心****,尤其是在持续用药4周后,心肌细胞促炎因子TNF2α表达水平降低,**因子IL210表达水平升高,TNF2α/IL210比值显著降低,同时监测这组大鼠心功能参数如左室舒张末期内径、射血分数、短轴缩短率和左室压力*大升降速率等皆明显改善。

实验结果显示芪苈强心胶囊减少心肌细胞促炎因子TNF2α和增加**因子IL210的**调节作用,可能是其部分改善心肌梗死大鼠心功能的**药理机制之一。

 

原文摘要:

Qiliqiangxin regulates the balance between tumor necrosisfactor-alpha and interleukin-10 and improves cardiac function inrats with myocardial infarction.
Xiao H, Song Y, Li Y, Liao YH, Chen J.

Laboratory of Cardiovascular Immunology, Institute of Cardiology,Union Hospital, Tongji Medical College of Huazhong University ofScience and Technology, Wuhan 430022, China.

Abstract
The study investigated the effects of traditional Chinese drugQiliqiangxin on cardiac function and the expression ofpro/anti-inflammatory cytokines TNF-alpha/IL-10 in rats withmyocardial infarction (MI). Rats with MI were randomly divided intodrug-treated group (MI-Q) and control group (MI-C) compared withsham-operated group (S). Rats in the MI-Q group were treated withcrude drug of oral Qiliqiangxin 24h after operation at the dosageof 4g/kg/day for 4weeks, while in MI-C group and S group weretreated with normal saline at the same time. Echocardiography andhemodynamic parameters, histopathologic changes and the expressionof myocardial cytokines including TNF-alpha and IL-10 were assessed4weeks after the drug therapy. The results indicated that rats ofthe MI-C group exhibited decreased cardiac function and increasedratio of TNF-alpha/IL-10 which principally secreted by myocardiumcompared with those of the S group and Qiliqiangxin treatmentsignificantly improved cardiac function and histopathologic changeswith down-regulated ratio of TNF-alpha/IL-10. These data suggeststhat Qiliqiangxin may improve cardiac function of rats with MIthrough regulation the balance between TNF-alpha and IL-10.