Xyloglucan intake attenuates myocardial injury by inhibiting apoptosis and improving energy metabolism in a rat model of myocardial infarction

2017 ◽  
Vol 45 ◽  
pp. 19-29 ◽  
Author(s):  
Sun Ha Lim ◽  
Jongwon Lee
Keyword(s):  
Myocardial Infarction ◽  
Energy Metabolism ◽  
Rat Model ◽  
Myocardial Injury

scholarly journals MicroRNA-322-5p Protects Against Myocardial Infarction through Targeting BTG2

2021 ◽  
Author(s):  
Yang Ruan ◽  
Shuai Meng ◽  
Ruofei Jia ◽  
Xiaojing Cao ◽  
zening Jin
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
B Cell ◽  
Rat Model ◽  
Myocardial Injury ◽  
Pathological Condition ◽  
Current Paper ◽  
Targeted Treatment ◽  
Myocardial Tissue

Abstract Objective: A large cohort of studies have addressed the therapeutic importance of microRNA (miR) in the treatment of myocardial infarction (MI). The current paper gives prominence to the role of miR-322-5p in MI by regulating B-cell translocation gene 2 (BTG2).Methods: In a rat model of MI miR-322-5p and BTG2 expression was estimated. Adenovirus that altered miR-322-5p or BTG2 expression was injected into MI rats. After that, cardiac function, inflammation, myocardial injury, pathological condition, apoptosis, and the NF-κB pathway-related genes in the myocardial tissue of MI rats after targeted treatment were evaluated. The targeting relationship between miR-322-5p and BTG2 was assessed.Results: miR-322-5p was lowly expressed and BTG2 was highly expressed in the myocardial tissue of MI rats. Restored miR-322-5p improved cardiac function, relived inflammation and myocardial injury, suppressed pathological condition and apoptosis and inactivated NF-κB pathway in MI rats. BTG2 expression was negatively mediated by miR-322-5p. Overexpressed BTG2 rescued miR-322-5p-induced cardioprotection on MI rats.Conclusion: It is evident that miR-322-5p protects against MI through suppressing BTG2 expression.

scholarly journals EFFECT OF MYOCARDIAL INFARCTION ON SPLEEN AND KIDNEY OF ISOPRENALINE-INDUCED MYOCARDIAL INJURY RAT MODEL

2019 ◽  
Vol 81 (2) ◽  
Author(s):  
Shafreena Shaukat Ali ◽  
Nur Hafiqah Rozalei ◽  
Siti Fatimah Azaharah Mohamed ◽  
Yap Wei Boon ◽  
Satirah Zainalabidin
Keyword(s):  
Myocardial Infarction ◽  
Rat Model ◽  
Myocardial Injury ◽  
Troponin T ◽  
Cardiac Injury ◽  
Early Time ◽  
Plasma Urea ◽  
Time Points ◽  
Function Test ◽  
Infarct Healing

Myocardial infarction (MI)-associated inflammation is crucial for post-infarct healing. However, unregulated inflammation may lead to unnecessary systemic inflammation, and affect other organs. This study investigated the effects of MI on spleen and kidneys over early time-points (2 and 7 days) in isoprenaline-induced MI rat model. MI was evident by elevated levels of cardiac injury marker, troponin T, and lactate dehydrogenase (LDH). MI rats showed significant upregulation of myeloperoxidase (MPO) activity at day-2 post infarct while kidney MPO activity remained unaffected. Kidney function test revealed only slightly increased plasma urea at day-2 post MI with no changes in plasma creatine at both time-points. Histological observation on the spleen showed disorganization of spleen structure at day-2 post MI while the kidney structures were preserved at both time-points. In conclusion, although MI-associated damages in the spleen were seen at day-2 post infarct, it had no impact on the kidney structures at both time-points.

Influence of sodium ferulate on miR-133a and left ventricle remodeling in rats with myocardial infarction

2020 ◽  
pp. 096032712095000
Author(s):  
Ganyang Li ◽  
Xiaohong Huang
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Rat Model ◽  
Myocardial Injury ◽  
Volume Fraction ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Sodium Ferulate ◽  
Left Ventricle Remodeling ◽  
Myocardial Infarction Size

To explore the influence of sodium ferulate (SF) on miR-133a and left ventricle remodeling (LVR) in rats with myocardial infarction (MI). The left coronary artery was ligated to create 36 ischemia-reperfusion (IR) rat models that were randomly divided into mock surgical group (MSG) (not ligated), model group (MG), and sodium ferulate group (SFG). After the successful modeling, SFG was intravenously injected with SF at the dose of 10 mg/kg, and the other two groups were injected with the same volume of normal saline. After 28 days, cardiac hemodynamic indices of all groups were measured; the myocardial infarction size (MIS), left ventricular mass index (LVMI), and collagen volume fraction (CVF) were calculated, the content of serum malondialdehyde (MDA) and activities of catalase (CAT), superoxide dismutase (SOD) and glutathione catalase (GSH-px) were detected by ELISA, and miR-133a expression in myocardial tissues of the left ventricle (LV) was detected by RT-qPCR. SF improved the cardiac hemodynamic indices of rat model and reduced the MIS, LVMI and CVF. SF decreased the serum MDA level and increased the serum CAT, SOD and GSH-px levels in rat model. SF increased the expression of miR-133a in myocardial tissue of rat model. Therefore, SF could effectively reduce the myocardial injury of IR rats and improve the LVR. Its mechanism may be related to the antioxygenation and upregulation of miR-133a.

Acute Myocardial Infarction in the Rat Model: Esmolol-Based Cardioplegia versus Potassium-Based Cardioplegia

2020 ◽  
Author(s):  
A. Veitinger ◽  
A. Komguem ◽  
M. Heep ◽  
B. Niemann ◽  
P. Grieshaber ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Rat Model

Mesenchymal Stem Cells Enhanced Cardiac Nerve Sprouting via Nerve Growth Factor in a Rat Model of Myocardial Infarction

2014 ◽  
Vol 20 (12) ◽  
pp. 2023-2029 ◽  
Author(s):  
Jian Chen ◽  
Shaoxin Zheng ◽  
Hui Huang ◽  
Suihua Huang ◽  
Changqing Zhou ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Rat Model ◽  
Nerve Growth ◽  
Cardiac Nerve ◽  
Nerve Sprouting

Regional Energy Metabolism of Failing Hearts Following Myocardial Infarction

1993 ◽  
Vol 25 (9) ◽  
pp. 995-1013 ◽  
Author(s):  
Atsushi Sanbe ◽  
Kouichi Tanonaka ◽  
Yumiko Hanaoka ◽  
Takashi Katoh ◽  
Satoshi Takeo
Keyword(s):  
Myocardial Infarction ◽  
Energy Metabolism ◽  
Regional Energy

scholarly journals Focal ST-segment elevation without coronary occlusion: myocardial infarction with no obstructive coronary atherosclerosis associated with COVID-19—a case report

2021 ◽  
Vol 5 (2) ◽  
Author(s):  
Casey Meizinger ◽  
Bruce Klugherz
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Respiratory Failure ◽  
Coronary Atherosclerosis ◽  
Myocardial Injury ◽  
Cardiovascular Complications ◽  
St Segment Elevation ◽  
St Segment ◽  
Hypoxic Respiratory Failure ◽  
Artery Disease

Abstract Background While it is understood that coronavirus disease 2019 (COVID-19) is primarily complicated by respiratory failure, more data are emerging on the cardiovascular complications of this disease. A subset of COVID-19 patients present with ST-elevations on electrocardiogram (ECG) yet normal coronary angiography, a presentation that can fit criteria for myocardial infarction with no obstructive coronary atherosclerosis (MINOCA). There is little known about non-coronary myocardial injury observed in patients with COVID-19, and we present a case that should encourage further conversation and study of this clinical challenge. Case summary An 86-year-old man presented to our institution with acute hypoxic respiratory failure and an ECG showing anteroseptal ST-segment elevation concerning for myocardial infarction. Mechanic ventilation was initiated prior to presentation, and emergent transthoracic echocardiography reported an ejection fraction of 50–55%, with no significant regional wall motion abnormalities. Next, emergent coronary angiography was performed, and no significant coronary artery disease was detected. The patient tested positive for COVID-19. Despite supportive management in the intensive care unit, the patient passed away. Discussion We present a case of COVID-19 that is likely associated with MINOCA. It is crucial to understand that in COVID-19 patients with signs of myocardial infarction, not all myocardial injury is due to obstructive coronary artery disease. In the case of COVID-19 pathophysiology, it is important to consider the cardiovascular effects of hypoxic respiratory failure, potential myocarditis, and significant systemic inflammation. Continued surveillance and research on the cardiovascular complications of COVID-19 is essential to further elucidate management and prognosis.

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