scholarly journals Protective effects of Yindanxinnaotong capsule in a rat model of myocardial ischemia/reperfusion injury

2014 ◽  
Vol 34 (6) ◽  
pp. 699-709 ◽  
Author(s):  
Wandan Wang ◽  
Lan Wang ◽  
Hongjun Yang ◽  
Jianlu Wang ◽  
Xiaojie Yin ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Protective effects of miR-34b and miR-337 against myocardial ischemia/reperfusion injury in rats by liposomal nano-delivery system

2021 ◽  
Vol 11 (7) ◽  
pp. 1147-1153
Author(s):  
Junyan Liu ◽  
Jingxian Xing ◽  
Ya Li ◽  
Juan Liu ◽  
Miao Tian ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sham Operation ◽  
Protective Effects ◽  
Expression Levels ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Although a few microRNAs (miRNAs) are involved in the regulation of myocardial ischemia/reperfusion injury (MI/RI), their exact roles in this process, and the mechanisms involved have not been fully elucidated. This study was carried out to investigate the protective effects of miR-34b and miR-337 against MI/RI. For this purpose, 56 Sprague-Dawley (SD) rats were randomly divided into two groups: sham operation group and myocardial MI/RI group, with 28 rats in each group. Then, a rat model of MI/RI was established. Changes in myocardial tissues of the two groups were determined using hematoxylin-Eosin (H&E) staining. Serum level of myocardial troponin c(TnT) was assayed with ELISA method, while myocardial tissue mRNA expressions of miR in the two groups was determined with qRT-PCR. Results showed that the rat model of MI/RI was successfully established, as was evident in myocardial cell necrosis, disorganized myocardial fibers, interstitial edema, and neutrophil infiltration. There were significant increases in serum troponin content and mRNA expression levels of miR-337 and miR-34b in tissues. In conclusion, the expression levels of miR-337 and miR-34b are increased in myocardial tissues of rats with MI/RI. Thus, miR-337 and miR-34b may be involved in the pathogenesis of MI/RI via regulation of NOX4 and Samd7, respectively. Finally, by using liposomal nanocarrier, the therapeutic effect of miR-337 and miR-34b on MI/RI was investigated.

scholarly journals The Cardioprotective Effects of Citric Acid and L-Malic Acid on Myocardial Ischemia/Reperfusion Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Xilan Tang ◽  
Jianxun Liu ◽  
Wei Dong ◽  
Peng Li ◽  
Lei Li ◽  
...  
Keyword(s):  
Citric Acid ◽  
Myocardial Ischemia ◽  
Organic Acids ◽  
Reperfusion Injury ◽  
Malic Acid ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Organic acids in Chinese herbs, the long-neglected components, have been reported to possess antioxidant, anti-inflammatory, and antiplatelet aggregation activities; thus they may have potentially protective effect on ischemic heart disease. Therefore, this study aims to investigate the protective effects of two organic acids, that is, citric acid and L-malic acid, which are the main components ofFructus Choerospondiatis, on myocardial ischemia/reperfusion injury and the underlying mechanisms. Inin vivorat model of myocardial ischemia/reperfusion injury, we found that treatments with citric acid and L-malic acid significantly reduced myocardial infarct size, serum levels of TNF-α, and platelet aggregation.In vitroexperiments revealed that both citric acid and L-malic acid significantly reduced LDH release, decreased apoptotic rate, downregulated the expression of cleaved caspase-3, and upregulated the expression of phosphorylated Akt in primary neonatal rat cardiomyocytes subjected to hypoxia/reoxygenation injury. These results suggest that both citric acid and L-malic acid have protective effects on myocardial ischemia/reperfusion injury; the underlying mechanism may be related to their anti-inflammatory, antiplatelet aggregation and direct cardiomyocyte protective effects. These results also demonstrate that organic acids, besides flavonoids, may also be the major active ingredient ofFructus Choerospondiatisresponsible for its cardioprotective effects and should be attached great importance in the therapy of ischemic heart disease.

Mechanism of decreased adenosine protection in reperfusion injury of aging rats

2000 ◽  
Vol 279 (1) ◽  
pp. H329-H338 ◽  
Author(s):  
Feng Gao ◽  
Theodore A. Christopher ◽  
Bernard L. Lopez ◽  
Eitan Friedman ◽  
Guoping Cai ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Protective Effects ◽  
No Release ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Cardioprotective Effects ◽  
Myocardial Ischemia Reperfusion

The purpose of this study was to determine whether the protective effects of adenosine on myocardial ischemia-reperfusion injury are altered with age, and if so, to clarify the mechanisms that underlie this change related to nitric oxide (NO) derived from the vascular endothelium. Isolated perfused rat hearts were exposed to 30 min of ischemia and 60 min of reperfusion. In the adult hearts, administration of adenosine (5 μmol/l) stimulated NO release (1.06 ± 0.19 nmol · min−1 · g−1, P < 0.01 vs. vehicle), increased coronary flow, improved cardiac functional recovery (left ventricular developed pressure 79 ± 3.8 vs. 57 ± 3.1 mmHg in vehicle, P < 0.001; maximal rate of left ventricular pressure development 2,385 ± 103 vs. 1,780 ± 96 in vehicle, P < 0.001), and reduced myocardial creatine kinase loss (95 ± 3.9 vs. 159 ± 4.6 U/100 mg protein, P < 0.01). In aged hearts, adenosine-stimulated NO release was markedly reduced (+0.42 ± 0.12 nmol · min−1 · g−1 vs. vehicle), and the cardioprotective effects of adenosine were also attenuated. Inhibition of NO production in the adult hearts significantly decreased the cardioprotective effects of adenosine, whereas supplementation of NO in the aged hearts significantly enhanced the cardioprotective effects of adenosine. The results show that the protective effects of adenosine on myocardial ischemia-reperfusion injury are markedly diminished in aged animals, and that the loss in NO release in response to adenosine may be at least partially responsible for this age-related alteration.

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