Effect of astragaloside on cardiac function,inflammatory-related cytokines and endothelial nitric oxide synthase signaling pathway in rats with acute myocardial infarction
10.7683/xxyxyxb.2018.03.002
- VernacularTitle:黄芪甲甙对急性心肌梗死大鼠早期心功能、炎性相关因子及内皮型一氧化氮合酶信号通路的影响
- Author:
Hao WANG
1
;
Shao-Xue WANG
;
Su-Min LI
;
Dong-Ming HAN
Author Information
1. 新乡医学院第一临床学院
- Keywords:
astragaloside;
acute myocardial infarction;
toll-like receptor;
endothelial nitric oxide synthase
- From:
Journal of Xinxiang Medical College
2018;35(3):167-172
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the cardio protective effect of astragaloside in rats with acute myocardial infarction and investigate the potential molecular mechanisms.Methods Forty-five Wistar rats were randomly divided into sham operation group,model group and astragaloside group,with 15 rats in each group.The acute myocardial infarction model was prepared by permanently occluding the left anterior descending artery in the model group and the astragaloside group,while the rats in the sham operation group were threaded only.Twenty-four hours after operation,the rats in the astragaloside group received astragaloside 20 mg · kg-1 · d-1 by intraperitoneal injection,once a day for two weeks.The rats in sham operation group and model group received isodose carboxymethylcellulose sodium by intraperitoneal injection,once a day for two weeks.Electrocardiogram was recorded to observe the changes of ST segment before ligation,after ligation immediately,1,3,7,14 d after intervened by astragaloside.Echocardiography was used to detect the left ventricular internal diameter at end-diastole (LVDD),left ventricular internal diameter at end-systole (LVDS),left ventricular end diastohc volume (LVEDV),left ventricular end systolic volume (LVESV),left ventricular fractional shortening (LVFS),left ventricular ejection fraction (LVEF).The levels of tumor necrosis factor alpha (TNF-α),interleukin (IL)-1 β,IL-6,nuclear factor-κB (NF-κB) in serum were measured by enzyme linked immunosorbent assay and the level of nitric oxide(NO) in plasma was measured by reagent kid.The expressions of toll-like receptor(TLR) 2,TLR4,nucleotide binding oligomerization do main(NOD) 1,NOD2,endothelial nitric oxide synthase (eNOS) mRNA were detected by quantitative real-time polymerase chain reaction.Results During the operation,there was 0,4,2 dead rats in the sham operation group,model group and astragaloside group.The ST segment in the model group and astragaloside group was higher than that in the sham operation group after operation immediately,1,3,7,14 d after intervented by astragaloside(P ＜ 0.01).The ST segment in the astragaloside group was lower than that in the model operation group at the time of 1,3,7,14 d after intervented by astragaloside(P ＜ 0.05).Compared with the sham operation group,the LVDD,LVDS,LVEDV,LVESV increased (P ＜ 0.01),LVFS,LVEF decreased (P ＜ 0.01),the levels of TNF-α,IL-1β,IL-6 and the expression of TLR2,TLR4,NOD1,NOD2 mRNA in cardiac muscle tissue were higher in the model group and astragaloside group (P ＜ 0.01),the level of NO was lower (P ＜ 0.05).The level of serum NF-κB in the model group was higher than that in the sham operation group(P ＜0.01),the expression of the eNOS mRNA in cardiac muscle tissue was lower than that in the sham operation group(P ＜ 0.05).There was no significant difference in the level of serum NF-κB and the expression of the eNOS mRNA in cardiac muscle tissue between the astragaloside group and sham operation group (P ＜ 0.05).Compared with the model group,in the astragaloside group the LVDD,LVDS,LVEDV,LVESV decreased (P ＜ 0.05),but LVFS,LVEF increased (P ＜ 0.05),the levels of TNF-o,IL-1 β,IL-6,NF-κB and the expression of TLR2,TLR4,NOD 1,NOD2 mRNA in cardiac muscle tissue were lower(P ＜ 0.05),the level of NO and the expression of the eNOS mRNA in cardiac muscle tissue were higher(P ＜ 0.05).Conclusion Astragaloside has protective effect against to acute myocardial infarction induced injury by decreasing the expression of TLR signal path and activating eNOS signaling.
