首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Electroacupuncture Pretreatment Regulates Apoptosis of Myocardial Ischemia-Reperfusion Injury in Rats Through RhoA/p38MAPK Pathway Mediated by miR-133a-5p
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Electroacupuncture Pretreatment Regulates Apoptosis of Myocardial Ischemia-Reperfusion Injury in Rats Through RhoA/p38MAPK Pathway Mediated by miR-133a-5p

机译:通过MIR-133A-5P介导的RHOA / P38MAPK途径调节大鼠心肌缺血再灌注损伤的细胞凋亡的预处理

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The electroacupuncture (EA) pretreatment possesses a beneficial effect on myocardial ischemia/reperfusion (I/R) injury. However, the molecular mechanism of the EA effect is not fully understood. The study aimed to explore the protective effect of EA pretreatment on myocardial ischemia-reperfusion injury (MIRI) and apoptosis-related mechanisms in rats. Rats underwent in vivo myocardial ischemia-reperfusion, EA pretreatment, or intravenous injection of antagomirs. Cardiac function, infarct area, and myocardial cell apoptosis were measured. Meanwhile, the expressions of MKK3, MKK6, p38MAPK, Bax, Bcl-2, and Caspase-3 were also detected. We found that EA pretreatment significantly reduced infarct area and myocarpal cell apoptosis and enhanced cardiac function. EA pretreatment decreased the expression of Bax, Caspase-3, MKK3, MKK6, p38MAPK, Bax, and Caspase-3. In conclusion, The EA pretreatment down regulated the expression of MKK3, MKK6, and p38MAPK through the RhoA/p38MAPK pathway. EA pretreatment protect MIRI rats from apoptosis by down regulating the expression of MKK3, MKK6, and p38MAPK, thereby reducing the expression of Bax, Caspase-3 and up regulating the expression of Bcl-2, which mechanism is closely related to the RhoA/p38MAPK pathway mediated by miR-133a-5p.
机译:电针(EA)预处理对心肌缺血/再灌注(I / R)损伤具有有益作用。然而,EA效应的分子机制尚未完全理解。该研究旨在探讨EA预处理对大鼠心肌缺血再灌注损伤(MiRI)和凋亡相关机制的保护作用。大鼠进行体内心肌缺血再灌注,EA预处理或静脉注射抗噬血症。测量心功能,梗塞区域和心肌细胞凋亡。同时,还检测了MKK3,MKK6,P38MAPK,BAX,BCL-2和Caspase-3的表达。我们发现EA预处理显着降低了梗塞区域和肌钙体细胞凋亡和增强的心功能。 EA预处理降低了Bax,Caspase-3,MKK3,MKK6,P38MAPK,BAX和Caspase-3的表达。总之,EA预处理通过RhoA / P38Mapk途径调节MKK3,MKK6和P38MAPK的表达。 EA预处理通过降低MKK3,MKK6和P38MAPK的表达,从而防止细胞凋亡免受细胞凋亡的影响,从而减少了Bax,Caspase-3和调节Bcl-2表达的表达,该机制与RhoA / P38Mapk密切相关由miR-133a-5p介导的途径。

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