| Autor: |
Naryzhnaya NV, Maslov IN, Khaliulin IG, Zhang Y, Pei JM, Tsepokina AV, Khutornaya MV, Kutikhin AG, Lishmanov YB |
| Jazyk: |
ruština |
| Zdroj: |
Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova [Ross Fiziol Zh Im I M Sechenova] 2016 Dec; Vol. 102 (12), pp. 1462-71. |
| Abstrakt: |
The study evaluated the role of protein kinase C, PI3-kinase and tyrosine kinases in the cardi-oprotective effect of the chronic continuous normobaric hypoxia (CCNH). Adaptation to CCNH was provided by placing the rats in an atmosphere with a low content of O2 (12 %) during 21 days. Anoxia-reoxygenation of isolated cardiomyocytes of intact rats caused the deaths of 16.5 % of the cells and the lactate dehydrogenase (LDH) release of them. A similar effect on isolated cardiomyocytes of adapted rats caused the death of only 6.8 % of the cells and less pronounced increase in LDH release. Preincubation of cells for 25 minutes with one of the protein kinases inhibitors: che-lerythrine (10 |mM/l); rottlerin (1 |j.M/l); genistein (50 |mM/l) eliminated the adaptive increase in cell survival and reduction of LDH release. Incubation of cells with PI3-kinase blocker wortman-nin (100 nM/l) had no effect on the percentage of cell death of adapted animals and LDH release from them after anoxia-reoxygenation. The authors believe that the cytoprotective effect of chronic normobaric hypoxia is realized through activation of protein kinase C-5 and tyrosine kinases. Kinase PI3 - is not involved in the implementation of protective actions CCNH. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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