Effect of Yuxingeng fluid on myocardial energy metabolism in Wistar rats with acute myocardial infarction

2004 ◽  
Vol 10 (1) ◽  
pp. 52-54
Author(s):  
Dong Guo-ju ◽  
Liu Jian-gang ◽  
Shi Da-zhuo
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Energy Metabolism ◽  
Wistar Rats ◽  
Myocardial Energy Metabolism

Abstract 332: Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Lichan Tao ◽  
Yihua Bei ◽  
Haifeng Zhang ◽  
Yanli Zhou ◽  
Jingfa Jiang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Energy Metabolism ◽  
Exercise Training ◽  
Mitochondrial Biogenesis ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Myocardial Infarct Size ◽  
Myocardial Energy Metabolism

Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury. However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. MI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.

scholarly journals Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

2015 ◽  
Vol 37 (1) ◽  
pp. 162-175 ◽  
Author(s):  
Lichan Tao ◽  
Yihua Bei ◽  
Shenghui Lin ◽  
Haifeng Zhang ◽  
Yanli Zhou ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Energy Metabolism ◽  
Exercise Training ◽  
Infarct Size ◽  
Mitochondrial Biogenesis ◽  
Myocardial Infarct ◽  
Immunofluorescent Staining ◽  
Myocardial Infarct Size ◽  
Myocardial Energy Metabolism

Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.

scholarly journals Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiu-ying Luo ◽  
Ze Zhong ◽  
Ai-guo Chong ◽  
Wei-wei Zhang ◽  
Xin-dong Wu
Keyword(s):  
Myocardial Infarction ◽  
Energy Metabolism ◽  
Ischemia Reperfusion ◽  
Heart Weight ◽  
Coronary Artery Ligation ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Myocardial Energy Metabolism ◽  
Atp Production ◽  
Ampk Pathway

Myocardial energy metabolism (MEM) is an important factor of myocardial injury. Trimetazidine (TMZ) provides protection against myocardial ischemia/reperfusion injury. The current study set out to evaluate the effect and mechanism of TMZ on MEM disorder induced by myocardial infarction (MI). Firstly, a MI mouse model was established by coronary artery ligation, which was then treated with different concentrations of TMZ (5, 10, and 20 mg kg–1 day–1). The results suggested that TMZ reduced the heart/weight ratio in a concentration-dependent manner. TMZ also reduced the levels of Bax and cleaved caspase-3 and promoted Bcl-2 expression. In addition, TMZ augmented adenosine triphosphate (ATP) production and superoxide dismutase (SOD) activity induced by MI and decreased the levels of lipid peroxide (LPO), free fatty acids (FFA), and nitric oxide (NO) in a concentration-dependent manner (all P < 0.05). Furthermore, an H2O2-induced cell injury model was established and treated with different concentrations of TMZ (1, 5, and 10 μM). The results showed that SIRT1 overexpression promoted ATP production and reactive oxygen species (ROS) activity and reduced the levels of LPO, FFA, and NO in H9C2 cardiomyocytes treated with H2O2 and TMZ. Silencing SIRT1 suppressed ATP production and ROS activity and increased the levels of LPO, FFA, and NO (all P < 0.05). TMZ activated the SIRT1–AMPK pathway by increasing SIRT1 expression and AMPK phosphorylation. In conclusion, TMZ inhibited MI-induced myocardial apoptosis and MEM disorder by activating the SIRT1–AMPK pathway.

Non-Q-wave myocardial infarction: impaired myocardial energy metabolism in regions with reduced 99mTc-MIBI accumulation

2001 ◽  
Vol 28 (5) ◽  
pp. 602-607 ◽  
Author(s):  
D. Moka ◽  
F.M. Baer ◽  
P. Theissen ◽  
C.A. Schneider ◽  
M. Dietlein ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Energy Metabolism ◽  
Myocardial Energy Metabolism ◽  
99Mtc Mibi ◽  
Q Wave
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