Diazoxide supplemented Celsior solution improves hypothermic heart preservation effect in rat through activation of mitochondrial ATP-sensitive potassium channel

Zhou, Yan; Hu, Zhibing; Pan, Xiaohua; Chen, Yingying; Zhang, Xiaoming; Shen, Yue‐Liang

doi:10.3109/13880200902991565

Cited by 5 publications

(1 citation statement)

References 20 publications

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“…Sprague-Dawley rats were anesthetized with 60 mg/kg sodium pentobarbital (intraperitoneal). The hearts were rapidly excised and washed in ice-cold KH solution, and mounted for retrograde perfusion using a modified Langendorff method (8). Following equilibration perfusion with KH solution (37˚C) for 30 min, the left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), maximal systolic velocity of left ventricular pressure (+dP/dt max ), maximal diastolic velocity of left ventricular pressure (-dP/dt max ) and heart rate were recorded as the basal value.…”

Section: In Vitro Hypothermic Heart Preservation Model Malementioning

confidence: 99%

Mechanism of uncoupling protein 2-mediated myocardial injury in hypothermic preserved rat hearts

Chen

Yan

Wang

et al. 2016

Molecular Medicine Reports

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In the present study, the alterations in uncoupling protein 2 (UCP2) expression following hypothermic preservation in rat hearts were investigated. Isolated rat hearts were preserved in Celsior solution for 3‑12 h followed by 60 min of reperfusion. The cardiac function was evaluated using the Langendorff perfusion system. UCP2 and silent mating type information regulation 2 homolog 1 (SIRT1) proteins were detected by western blot analysis. The ATP production and mitochondrial reactive oxygen species (ROS) levels were assessed. Subsequent to preservation in ice‑cold Celsior solution for 3‑12 h, the UCP2 protein expression in rat hearts was observed to increase in a time‑dependent manner. The UCP2 inhibitor genipin inhibited the hypothermic preservation‑induced cardiac dysfunction, prevented a decline in ATP production induced by 9 h of preservation, however had no effect on the hypothermic preservation‑induced increase in mitochondrial ROS levels. Compared with the control group, the SIRT1 protein expression in rat hearts reduced following hypothermic preservation. Compared with the 9‑h preservation group, Celsior solution supplemented with the SIRT1 activator resveratrol (20 or 40 µmol/l) inhibited UCP2 protein overexpression, prevented the decline in ATP production and resulted in an improvement cardiac function. The SIRT1 inhibitor EX‑527 abolished the resveratrol‑induced inhibition of UCP2 overexpression and cardiac protection in the hypothermic preserved rat heart. These observations suggest that downregulation of UCP2 expression in the hypothermic preserved rat heart in part initiated the protective mechanism via the SIRT1 pathway.

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Section: In Vitro Hypothermic Heart Preservation Model Malementioning

confidence: 99%

Mechanism of uncoupling protein 2-mediated myocardial injury in hypothermic preserved rat hearts

Chen

Yan

Wang

et al. 2016

Molecular Medicine Reports

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Heat shock protein 90 mediates anti-apoptotic effect of diazoxide by preventing the cleavage of Bid in hypothermic preservation rat hearts

Yang

Chen

Zheng

et al. 2011

The Journal of Heart and Lung Transplantation

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Lipopolysaccharide pretreatment promotes cardiac stem cell migration through heat shock protein 90-dependent β-catenin activation

Zhang

Geng

et al. 2016

Life Sciences

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Diazoxide supplemented Celsior solution improves hypothermic heart preservation effect in rat through activation of mitochondrial ATP-sensitive potassium channel

Abstract: (2009) Diazoxide supplemented Celsior solution improves hypothermic heart preservation effect in rat through activation of mitochondrial ATP-sensitive potassium channel,

Cited by 5 publications

References 20 publications

Mechanism of uncoupling protein 2-mediated myocardial injury in hypothermic preserved rat hearts

Mechanism of uncoupling protein 2-mediated myocardial injury in hypothermic preserved rat hearts

Heat shock protein 90 mediates anti-apoptotic effect of diazoxide by preventing the cleavage of Bid in hypothermic preservation rat hearts

Lipopolysaccharide pretreatment promotes cardiac stem cell migration through heat shock protein 90-dependent β-catenin activation

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