Urocortin inhibits Beclin1-mediated autophagic cell death in cardiac myocytes exposed to ischaemia/reperfusion injury

2006 ◽  
Vol 40 (6) ◽  
pp. 846-852 ◽  
Author(s):  
Lauren Valentim ◽  
Kevin M. Laurence ◽  
Paul A. Townsend ◽  
Christopher J. Carroll ◽  
Surinder Soond ◽  
...  
2016 ◽  
Vol 130 (18) ◽  
pp. 1641-1653 ◽  
Author(s):  
Yuanna Ling ◽  
Guiming Chen ◽  
Yi Deng ◽  
Huixiong Tang ◽  
Long Ling ◽  
...  

The present paper provides evidence that polydatin (PD) post-treatment alleviates myocardial ischaemia/reperfusion (I/R) injury by promoting autophagic flux to clear damaged mitochondria to reduce reactive oxygen species (ROS) and cell death.


Metallomics ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1330-1343 ◽  
Author(s):  
Joseph Ischia ◽  
Damien M. Bolton ◽  
Oneel Patel

Ischaemia (interruption in the blood/oxygen supply) and subsequent damage induced by reperfusion (restoration of blood/oxygen supply) ultimately leads to cell death, tissue injury and permanent organ dysfunction.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Héctor González-Pacheco ◽  
Aurelio Méndez-Domínguez ◽  
Salomón Hernández ◽  
Rebeca López-Marure ◽  
Maria J. Vazquez-Mellado ◽  
...  

Background. CDP-choline is a key intermediate in the biosynthesis of phosphatidylcholine, which is an essential component of cellular membranes, and a cell signalling mediator. CDP-choline has been used for the treatment of cerebral ischaemia, showing beneficial effects. However, its potential benefit for the treatment of myocardial ischaemia has not been explored yet.Aim. In the present work, we aimed to evaluate the potential use of CDP-choline as a cardioprotector in anin vitromodel of ischaemia/reperfusion injury.Methods. Neonatal rat cardiac myocytes were isolated and subjected to hypoxia/reperfusion using the coverslip hypoxia model. To evaluate the effect of CDP-choline on oxidative stress-induced reperfusion injury, the cells were incubated with H2O2during reperfusion. The effect of CDP-choline pre- and postconditioning was evaluated using the cell viability MTT assay, and the proportion of apoptotic and necrotic cells was analyzed using the Annexin V determination by flow cytometry.Results. Pre- and postconditioning with 50 mg/mL of CDP-choline induced a significant reduction of cells undergoing apoptosis after hypoxia/reperfusion. Preconditioning with CDP-choline attenuated postreperfusion cell death induced by oxidative stress.Conclusion. CDP-choline administration reduces cell apoptosis induced by oxidative stress after hypoxia/reperfusion of cardiac myocytes. Thus, it has a potential as cardioprotector in ischaemia/reperfusion-injured cardiomyocytes.


Oncotarget ◽  
2016 ◽  
Vol 7 (26) ◽  
pp. 39345-39362 ◽  
Author(s):  
Yuesheng Xia ◽  
Yan Liu ◽  
Tong Xia ◽  
Xing Li ◽  
Cong Huo ◽  
...  

Gut ◽  
1998 ◽  
Vol 42 (4) ◽  
pp. 530-537 ◽  
Author(s):  
H Ikeda ◽  
Y Suzuki ◽  
M Suzuki ◽  
M Koike ◽  
J Tamura ◽  
...  

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