黄芪甲苷对脂多糖诱导的小鼠脓毒症心肌病及过氧化物酶体增殖物激活受体α的影响

doi:10.13418/j.issn.1001-165x.2020.02.017

中国临床解剖学杂志 ›› 2020, Vol. 38 ›› Issue (2): 189-193.doi: 10.13418/j.issn.1001-165x.2020.02.017

黄芪甲苷对脂多糖诱导的小鼠脓毒症心肌病及过氧化物酶体增殖物激活受体α的影响

聂取^{1, 2}，　李梦非²，　王洪新²

1.锦州医科大学附属第一医院，辽宁锦州 121001； 2.锦州医科大学药理教研室，辽宁锦州 121001

收稿日期:2019-02-26 出版日期:2020-03-25 发布日期:2020-04-01
通讯作者: 王洪新，教授，博士，硕士研究生导师，E-mai：jyhxwang@163.com
作者简介:聂取（1985-），女，辽宁锦州人，硕士，研究方向：心血管药理学，E-mail：253708405@qq.com
基金资助:
辽宁省自然科学基金（201602317）

Effects of Astragaloside IV on sepsis myocardiopathy and peroxisomal proliferate activation receptor alpha in mice induced by lipopolysaccharide

NIE Qu^1,2, LI Meng-fei²，WANG Hong-xin²

1. The First Affiliated Hospital of Jinzhou Medical University，Jinzhou 121001, China; 2. Department of Pharmacology, Jinzhou Medical University，Jinzhou 121001, China

Received:2019-02-26 Online:2020-03-25 Published:2020-04-01

摘要/Abstract

摘要： 目的　探讨黄芪甲苷（Astragaloside IV，ASIV）对脂多糖（lipopolysaccharide，LPS）诱导的小鼠脓毒症心肌病及过氧化物酶体增殖物激活受体α（PPARα）的影响。方法　50只健康雄性C57BL/6J小鼠随机分为5组，每组10只，分为空白对照组、脂多糖模型组、ASIV（20、40、80 mg·kg-1·d-1）组。ASIV组灌胃ASIV 7 d，然后同模型组给予脂多糖10 mg/kg一次性腹腔注射建立急性内毒素损伤模型。8 h后超声观察小鼠心功能指标：射血分数（EF）、缩短分数（FS）、左心室舒张末期内径（LVIDd）、左心室收缩末期内径（LVIDs）；HE染色观察小鼠心脏组织形态学变化；酶联免疫吸附测定肿瘤坏死因子（TNF- α）、白介素-1β（IL-1β）、白介素-6（IL-6）、游离脂肪酸（FFA）的表达水平；高效液相色谱法检测三磷酸腺苷（ATP）、二磷酸腺苷（ADP）、单磷酸腺苷（AMP）的含量；Western blot法检测心肌组织中PPARα、ATP5D的蛋白表达水平。结果　与模型组相比，ASIV组的心功能指标EF、FS、LVIDd、LVIDs提高，改善了心肌组织的炎性细胞浸润、心肌纤维变形，TNF-α、IL-1β、IL-6、FFA的表达减少，ATP/AMP、ADP/AMP比值增加，PPARα、ATP5D的蛋白表达增多。结论　ASIV可能是通过PPAR改善脂多糖诱导的心肌损伤能量代谢水平，对脓毒症心肌病起到保护作用。

关键词: ASIV, 　脂多糖, 　脓毒症心肌病, 　过氧化物酶体增殖物激活受体α, 　能量代谢

Abstract: Objective To investigate the effects of Astragaloside IV (ASIV) on myocardial myocardiopathy and peroxisomal proliferate activation receptor α (PPARα) in mice induced by lipopolysaccharide (LPS).　Methods　50 healthy male C57BL/6J mice were randomly divided into 5 groups, each group of 10 mice, which were divided into a blank control group, a lipopolysaccharide model group and three astragaloside IV (20, 40, 80 mg/kg/d) groups. Astragaloside IV was administered to the ASIV groups for 7 days, and then the model group was given LPS (10 mg/kg) to establish an acute endotoxin damage model. After 8 h, ultrasound was used to observe the mouse heart function index: ejection fraction (EF), shortening fraction (FS), left ventricular diastolic inner diameter (LVIDd), and left ventricular end-systolic diameter (LVIDs); HE staining was used to observe the morphological changes of the heart tissue of mice; Enzyme linked immunosorbent assay (ELISA) was used to detect tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and free fatty acid (FFA); High performance liquid chromatography (HPLC) was used to detect the content of adenosine triphosphate (ATP), adenosine diphosphate(ADP) and adenosine monophosphate (AMP); Western Blot was used to detect the protein expression levels of PPARα and ATP5D in myocardial tissues. 　Results　Compared with the model group, the increasing of the cardiac function index EF, FS, LVIDd and LVIDs of the ASIV groups improved the infiltration of inflammatory cells and the deformation of myocardial fibers, decreased the content of TNF-α, IL-1β, IL-6, FFA, and increased the ratio of ATP/AMP and ADP/AMP ; increased the protein expressions of PPARα and ATP5D.　Conclusions　Astragaloside IV may be used to improve the energy metabolism of myocardial injury induced by lipopolysaccharide by PPARα, which can protect the cardiomyopathy of sepsis.

Key words: , Astragaloside IV, 　Lipopolysaccharide, 　Sepsis cardiomyopathy, 　PPARα, 　Energy metabolism

中图分类号:

R963

聂取, 李梦非, 王洪新. 黄芪甲苷对脂多糖诱导的小鼠脓毒症心肌病及过氧化物酶体增殖物激活受体α的影响[J]. 中国临床解剖学杂志, 2020, 38(2): 189-193.

NIE Qu, LI Meng-fei, WANG Hong-xin. Effects of Astragaloside IV on sepsis myocardiopathy and peroxisomal proliferate activation receptor alpha in mice induced by lipopolysaccharide[J]. Chinese Journal of Clinical Anatomy, 2020, 38(2): 189-193.

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黄芪甲苷对脂多糖诱导的小鼠脓毒症心肌病及过氧化物酶体增殖物激活受体α的影响

Effects of Astragaloside IV on sepsis myocardiopathy and peroxisomal proliferate activation receptor alpha in mice induced by lipopolysaccharide

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