Naloxone delays the collapse of mitochondrial membrane potential in cultured myocardial cell induced by hypoxia/reoxygenation.
Sha Wang
Abstract
Sha Wang
Abstract
Objective:To study the protective effect of Nalonxe on mitochondrial membrane potential in cultured myocardial cell after hypoxia. Methods:Cultured rabbit's myocardial cell was divided in three groups(control, hypoxia/reoxygenation group , hypoxia/reoxygenation combined with Naloxone therapy group) and the latter tow groups were further divided into three subsections: hypoxia 2 hour, hypoxia 2h/reoxygen 2h, hypoxia 2h/reoxygen 4h.. At the end of intervention, the cells were stained with JC-1(5,5',6,6'-tetrachloro-1,1 ',3,3 '-tetrethyl benzimidalyl carbocyanine iodide) and mitochondrial membrane potential (m) was assayed by flow cytometry . Results:(1)After intervention, the m of each subsection was lower than the control, and the naloxone therapy group was higher than the hypoxia/reoxygenation group (P0.01) (2)A remarkable losing of m occurred during reoxygenation period,but not hypoxia. (3)The sharp deceasing of m in Naloxone therapy group was later than the hypoxia/reoxygenation group. Conclusions:Hypoxia/reoxygenation may lead to the collapse of mitochondrial membrane potential in cultured myocardial cell. Naloxone may significantly mitigate and delay this loss.
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Objective:To study the protective effect of Nalonxe on mitochondrial membrane potential in cultured myocardial cell after hypoxia. Methods:Cultured rabbit's myocardial cell was divided in three groups(control, hypoxia/reoxygenation group , hypoxia/reoxygenation combined with Naloxone therapy group) and the latter tow groups were further divided into three subsections: hypoxia 2 hour, hypoxia 2h/reoxygen 2h, hypoxia 2h/reoxygen 4h.. At the end of intervention, the cells were stained with JC-1(5,5',6,6'-tetrachloro-1,1 ',3,3 '-tetrethyl benzimidalyl carbocyanine iodide) and mitochondrial membrane potential (m) was assayed by flow cytometry . Results:(1)After intervention, the m of each subsection was lower than the control, and the naloxone therapy group was higher than the hypoxia/reoxygenation group (P0.01) (2)A remarkable losing of m occurred during reoxygenation period,but not hypoxia. (3)The sharp deceasing of m in Naloxone therapy group was later than the hypoxia/reoxygenation group. Conclusions:Hypoxia/reoxygenation may lead to the collapse of mitochondrial membrane potential in cultured myocardial cell. Naloxone may significantly mitigate and delay this loss.
Key concepts: Hypoxia (environmental), Membrane potential, Cell, Flow cytometry, Mitochondrion, Inner mitochondrial membrane, Internal medicine, Biology