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1. 南京中医药大学针药结合教育部重点实验室
2. 南京中医药大学附属医院
纸质出版日期:2022
移动端阅览
杨文秀, 陈栎遥, 杨嘉丽, 等. 不同强度电针预处理对急性心肌缺血小鼠心功能及巨噬细胞极化的影响[J]. 针刺研究, 2022,47(11):955-961.
YANG Wen-xiu, CHEN Li-yao, YANG Jia-li, et al. Effect of different electrical current intensities of electroacupuncture preconditioning on cardiac function and macrophage polarization in mice with acute myocardial ischemia[J]. Acupuncture research, 2022, 47(11): 955-961.
杨文秀, 陈栎遥, 杨嘉丽, 等. 不同强度电针预处理对急性心肌缺血小鼠心功能及巨噬细胞极化的影响[J]. 针刺研究, 2022,47(11):955-961. DOI: 10.13702/j.1000-0607.20211011.
YANG Wen-xiu, CHEN Li-yao, YANG Jia-li, et al. Effect of different electrical current intensities of electroacupuncture preconditioning on cardiac function and macrophage polarization in mice with acute myocardial ischemia[J]. Acupuncture research, 2022, 47(11): 955-961. DOI: 10.13702/j.1000-0607.20211011.
目的:观察不同强度电针预处理对急性心肌缺血(AMI)小鼠心功能影响的效应差异,并探讨其可能的作用机制。方法:C57BL/6J小鼠随机分为假手术组、模型组、电针预处理组(0.5 mA组、1 mA组、3 mA组)
每组10只。各电针预处理组采用0.5、1、3 mA电流强度分别电针小鼠双侧“内关”
每次20 min
每日1次,连续干预3 d后造模。采用结扎心脏冠状动脉左前降支法建立AMI小鼠模型。采用超声心动评价各组小鼠心脏功能,TTC染色法检测心肌梗死面积百分比,流式细胞技术检测心脏巨噬细胞数量和M1/M2巨噬细胞极化状态,Western blot法检测心肌组织白细胞介素-1β(IL-1β)、肿瘤坏死因子α(TNF-α)、Toll样受体4(TLR4)蛋白表达水平。结果:与假手术组比较,模型组左心室射血分数(EF)和短轴收缩率(FS)降低(P<0.000 1)
心肌梗死面积百分比升高(P<0.000 1)
心脏巨噬细胞数量增加(P<0.000 1)
且以M1型为主,心肌组织IL-1β、TNF-α、TLR4蛋白表达水平升高(P<0.001
P<0.01)。与模型组比较,0.5 mA组、1 mA组和3 mA组EF和FS均明显升高(P<0.000 1
P<0.05
P<0.001)
心肌梗死面积百分比明显降低(P<0.000 1
P<0.01)
心肌组织IL-1β、TNF-α、TLR4蛋白表达水平均降低(P<0.01
P<0.05
P<0.001)
1 mA组心脏巨噬细胞数量降低(P<0.05)
且以M1型为主。与1 mA组比较,0.5 mA组和3 mA组EF和FS降低(P<0.01
P<0.000 1)
心肌梗死面积百分比升高(P<0.01
P<0.000 1)
心肌组织TLR4蛋白表达水平升高(P<0.01)
0.5 mA组心肌组织IL-1β、TNF-α蛋白表达水平升高(P<0.05)。结论:0.5、1、3 mA电针预处理均能有效改善AMI小鼠心功能,减少AMI小鼠心肌梗死面积和心脏巨噬细胞数量,下调心肌组织IL-1β、TNF-α、TLR4蛋白表达;其中1 mA组效应最佳,可能与其促进心肌巨噬细胞由M1型向M2型极化有关。
Objective To observe the effect of different intensities of electroacupuncture(EA) preconditioning on car-diac function and polarization state of macrophages in mice with acute myocardial ischemia(AMI)
so as to explore its possible mechanism underlying improvement of AMI. Methods A total of 50 male C57 BL/6 J mice were randomly divided into sham ope-ration
AMI model
and EA pretreatment groups(0.5 mA
1 mA
3 mA subgroups)
with 10 mice in each group/subgroup. The mice in the EA pretreatment groups were subjected to EA stimulation of bilateral “Neiguan”(PC6) with 0.5
1.0 and 3 mA respectively and frequency of 2 Hz/15 Hz for 20 min
once a day
for 3 days. The acute myocardial ischemia model was established by ligating the anterior descending branch(ADB) of the left coronary artery
while the sham operation only had a surgical suture trans-passed below the ADB but without ligation. The myocardial infarction area was measured after TTC staining
and the cardiac function [left ventricular ejection fraction(EF)
short-axis contraction rate(FS)] was detected by using echocardiography. The M1 macrophages were labeled with CD11 b+F480+CD206
(low)
M2 macrophages were labeled with CD11 b+F480+CD206(low)
M2 macrophages were labeled with CD11 b+F480+CD206
(high)
and detected by using flow cytometry
and the expression levels of myocardial interleukin-1β(IL-1β)
tumor necrosis factor-α(TNF-α)
Toll-like receptor-4(TLR4) proteins were detected by using Western blot. Results Compared with the sham operation group
the model group had a significant increase in the infarction area(P
<
0.000 1)
number of cardiac macrophages and percentage of M1 type macrophages(P
<
0.000 1)
and the expression levels of myocardial IL-1β
TNF-α
TLR4 proteins(P
<
0.001
P
<
0.01)
and a remarkable decrease in the levels of EF
FS and the percentage of M2 type macrophages(P
<
0.000 1). In contrast to those of the model group
the area of myocardial infarction(P
<
0.000 1
P
<
0.01)
expression levels of myocardial IL-1β
TNF-α
TLR4 proteins(P
<
0.01
P
<
0.05
P
<
0.001) in the 0.5 mA
1 mA and 3 mA groups
number of macrophages and percentage of M1 macrophages(P
<
0.05) in the 1 mA group were significantly decreased
while the levels of EF and FS(P
<
0.000 1
P
<
0.05
P
<
0.001) in the 3 EA groups
and percentage of M2 macrophage(P
<
0.05) in the 1 mA group were significantly increased. Comparison among the 3 EA groups displayed that the effects of 1 mA group were significantly superior to those of 0.5 and 3 mA groups in up-regulating EF and FS(P
<
0.01
P
<
0.001)
and in down-regulating the area of infarct myocardium(P
<
0.01
P
<
0.000 1)
and the expression of TLR4 protein(P
<
0.01)
and 0.5 mA group in the expression of IL-1β and TNF-α proteins(P
<
0.05). Conclusion EA preconditioning with electrical current intensities of 0.5 mA
1 mA and 3 mA can effectively reduce myocardial infarction size
improve cardiac function in mice with AMI
which may be related with its effects in reducing the number of cardiac macrophages and down-regulating the expression of myocardial IL-1β
TNF-α and TLR4 proteins. The therapeutic effect of 1 mA is better than that of 0.5 and 3 mA.
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