Streptozotocin-induced type II diabetic rat administered with nonobesogenic high-fat diet is highly susceptible to myocardial ischemia-reperfusion injury: An insight into the function of mitochondria

2018 ◽  
Vol 234 (4) ◽  
pp. 4104-4114 ◽  
Author(s):  
Mahalakshmi Ansari ◽  
Senthilkumar Gopalakrishnan ◽  
Gino A. Kurian
Keyword(s):  
Myocardial Ischemia ◽  
High Fat Diet ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rat ◽  
Type Ii ◽  
High Fat ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Insight Into

Insight into long noncoding RNA–miRNA–mRNA axes in myocardial ischemia-reperfusion injury: the implications for mechanism and therapy

Epigenomics ◽  
2019 ◽  
Vol 11 (15) ◽  
pp. 1733-1748 ◽  
Author(s):  
Wei Xiong ◽  
Yan Qu ◽  
Hongmei Chen ◽  
Jinqiao Qian
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Noncoding Rnas ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Insight Into

Emerging evidence has demonstrated that regulatory noncoding RNAs (ncRNAs), such as long noncoding RNAs (lncRNAs) and miRNAs, play crucial roles in the initiation and progress of myocardial ischemia-reperfusion injury (MIRI), which is associated with autophagy, apoptosis and necrosis of cardiomyocytes, as well as oxidative stress, inflammation and mitochondrial dysfunction. LncRNAs serve as a precursor or host of miRNAs and directly/indirectly affecting miRNAs via competitive binding or sponge effects. Simultaneously, miRNAs post-transcriptionally regulate the expression of genes by targeting various mRNA sequences due to their imperfect pairing with mRNAs. This review summarizes the potential regulatory role of lncRNA–miRNA–mRNA axes in MIRI and related molecular mechanisms of cardiac disorders, also provides insight into the potential therapies for MIRI-induced diseases.

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 NARINGIN ATTENUATES OXIDATIVE STRESS AND PROTECT AGAINST MYOCARDIAL ISCHEMIA-REPERFUSION INJURY IN DIABETIC RAT

2019 ◽  
pp. 230-234
Author(s):  
NEELAM KUMARI ◽  
AJAY SINGH KUSHWAH
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
The Body ◽  
Diabetic Rat ◽  
Diabetic Patients ◽  
Coronary Artery Ligation ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Objective: The relative risk of coronary heart disease in diabetic patients is more than in non-diabetic population. The present study was undertaken to explore the cardioprotective effect of Naringin on ischemia-reperfusion injury in the diabetic model of rat. Methods: Adult Wistar rats (either sex) divided into six groups. Diabetes was induced by 5 weeks combine exposure to a high-fat diet with a low dose of streptozotocin (30 mg/kg i.p.), administered on the 1st day of starting of the 5th week. Naringin treatment 25 mg/kg and 50 mg/kg was given simultaneously for 5 weeks. On the 36th day, the study animals were subjected to induction myocardial ischemia-reperfusion injury induced by the ligation of the left anterior descending coronary artery ligation in anesthetizing rat. Serum glucose level and cholesterol level measured before performing of ischemic reperfusion. After reperfusion injury, the animals were sacrificed and estimate change in the heart in the course of biochemical alterations, in creatine kinase-muscle/ brain (CK-MB) and lactate dehydrogenase, lipid peroxidation (LPO), glutathione (GSH), superoxide dismutase (SOD) and infarct size in the heart. Results and Conclusion: Naringin treatment significantly reduced the body weight, blood glucose, cholesterol, cardiac injury biomarkers, and LPO level and increased in antioxidant (GSH and SOD) level and also significantly increased in mean arterial pressure heart rate, reduced the myocardial infarction size. The present study concludes that Naringin 50 mg/kg being more prominent action to reduce the cardiotoxicity risk in ischemia-reperfusion injury state and increases myocardial susceptibility through having more prominent antioxidant potential properties.

Sign in / Sign up

Export Citation Format

Share Document