scholarly journals Electroacupuncture Pretreatment Regulates Apoptosis of Myocardial Ischemia-Reperfusion Injury in Rats Through RhoA/p38MAPK Pathway Mediated by miR-133a-5p

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Yongli Han ◽  
Song Chen ◽  
Hua Wang ◽  
Xing-ming Peng
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Infarct Area ◽  
P38mapk Pathway ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

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.

scholarly journals MicroRNA-24-3p Attenuates Myocardial Ischemia/Reperfusion Injury by Suppressing RIPK1 Expression in Mice

2018 ◽  
Vol 51 (1) ◽  
pp. 46-62 ◽  
Author(s):  
Hong Tan ◽  
Jie Qi ◽  
Bo-Yuan Fan ◽  
Jian Zhang ◽  
Fei-Fei Su ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Mouse Model ◽  
Cardiac Function ◽  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Infarct Area ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Background/Aims: This study was developed to investigate a potential therapeutic method for myocardial ischemia/reperfusion injury involving the promotion of miR-24-3p expression. Methods: Microarray analysis was used to screen differentially expressed genes in a myocardial ischemia/reperfusion (I/R) injury mouse model. Gene set enrichment analysis was utilized to determine vital signaling pathways. Targeting verification was conducted with a luciferase reporter assay. Myocardial I/R injury was developed in mice, and the expression levels of RIPK1 and miR-24-3p were investigated by qRT-PCR and Western blot. Hemodynamic parameters and the activity of serum myocardial enzymes were measured to evaluate cardiac function. Infarct area was observed through HE and TTC staining. Myocardial cell apoptosis was examined by TUNEL staining and caspase-3 activity analysis. Results: RIPK1 was an upregulated mRNA found by microarray analysis and a verified target of the downregulated miRNA miR-24-3p. The upregulation of RIPK1 (1.8-fold) and the downregulation of miR-24-3p (0.3-fold) were confirmed in I/R mice. RIPK1 led to impaired cardiac function indexes, increased infarct area and cell apoptosis, while miR-24-3p could reverse the injury by regulating RIPK1. The TNF signaling pathway was proven to be involved in myocardial I/R injury through the detection of the dysregulation of related proteins. Conclusion: In conclusion, RIPK1 was upregulated and miR-24-3p was downregulated in a myocardial I/R injury mouse model. RIPK1 could aggravate myocardial I/R injury via the TNF signaling pathway, while miR-24-3p could suppress RIPK1 and therefore exert cardioprotective effects in myocardial I/R injury.

scholarly journals 5′-N-Ethylcarboxamido Adenosine Attenuates Myocardial Ischemia/Reperfusion Injury In Type 2 Diabetic Rats Through A2AR/PKCα/miR-15a Signaling

2021 ◽  
Author(s):  
Chao Chen ◽  
Jianjuan Ke ◽  
Huang Ding ◽  
Chengjun Hu ◽  
Zhenggang Wang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Caspase 3 ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rat ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Type 2 Diabetic

Abstract Background/aims: Type 2 diabetes mellitus aggravates myocardial ischemia/reperfusion injury (MI/RI). Activation of adenosine receptors (ARs) confer to attenuated MI/RI in nondiabetic animals and human. However, this effects and mechanism of ARs in the type 2 diabetic state are still unknown. In present study, we established a type 2 diabetic rat in vivo myocardial ischemia/reperfusion (MI/R) model to evaluate the effect of ARs on MI/RI with a focus on the A2A adenosine receptor (A2 AR) -mediated cardioprotective effects. Methods: Type 2 diabetic rat were subjected to myocardial infarction by LAD ligation in situ and randomly received ARs agonist and/or antagonists or vehicle treatment. After 2h marker of the extent of myocardial damage(ejection fraction of the LV, Infarct size, plasma cardiac troponin I) were measured and pro- and anti-apoptotic signals (protein kinase Cα，Bcl-2, Bax, miR-15), and marker of apoptosis execution (cleaved caspase-3, TUNEL) were quantified in the infarcted myocardium.Results: non-selective adenosine receptor agonist 5′-(N-ethylcarboxamido) adenosine treatment attenuates MI/RI, improve post-MI/R left ventricular function, limit infarct size, reduce cardiac troponin I release, reduce myocardial apoptosis, up-regulates bcl2 and down-regulates miR-15a, bax and cleaved caspase-3 expression; This protective effects were attenuated by pretreatment with selective A2AR antagonist ZM241385 or PKCα-selective inhibitor Go6976; and duplicated by treatment with A2AR-selective agonist CGS21680 or PKCα-potent activator PMA.Conclusions: NECA reduces MI/RI in T2DM rats via the A2AR/PKCα/miR-15a signaling pathway; NECA is a useful target candidate for the treatment of MI/RI in patient with type 2diabetes.

scholarly journals LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88

2021 ◽  
Author(s):  
Feng Gao ◽  
Xiaochen Wang ◽  
Tingting Fan ◽  
Zhidan Luo ◽  
Mengqin Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Primary Response ◽  
Cardiomyocyte Apoptosis ◽  
Non Coding Rna ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Abstract Objective Long non-coding RNA (lncRNA) play critically in myocardial ischemia-reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis. Methods Mice with I/R injury were injected with the vectors that altered miR-185-3p and LINC00461 expression. miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury were measured, as well as cardiac function, hemodynamics, myocardial fibrosis, infarction area, oxidative stress, and cardiomyocyte apoptosis. Results Raised LINC00461 and Myd88 and suppressed miR-185-3p levels were measured in I/R mice. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial collagen hyperplasia, fibrosis and infarction, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. Conclusion Down-regulation of LINC00461 attenuates myocardial I/R injury via suppressing miR-185-3p-targeted Myd88 expression.

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