期刊
BRAIN RESEARCH BULLETIN
卷 103, 期 -, 页码 66-71出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2014.02.008
关键词
Adenosine A1 receptor; Akt; Inter-cell preconditioning; Neuroprotection
资金
- National Institutes of Health, Bethesda, Maryland, from the International Anesthesia Research Society [R01 GM065211, R01 GM098308]
- Cleveland, Ohio, from the American Heart Association Mid-Atlantic Affiliate, Baltimore, Maryland [10GRNT3900019]
- Robert M. Epstein Professorship Endowment, University of Virginia
Ischemic preconditioning-induced neuroprotection is a well-known phenomenon. We hypothesize that this form of neuroprotection is transferable among the same type of cells. To test this hypothesis, human neuroblastoma SH-SY5Y cells were induced to become neuron-like cells. Primary rat cortical neuronal cultures were also used. These cells were subjected to various lengths of short oxygen-glucose deprivation (OGD, an in vitro simulation of ischemia) and then 1-h OGD. Some cells that were not exposed to a short episode of ischemia were incubated with culture medium from the cells that had 3- or 5-min OGD. Those cells were subjected to OGD for 1 h at 1 or 24 h after they were exposed to the medium. Cell injury was evaluated at 24 h after the 1-h OGD by lactate dehydrogenase release assay. In another experiment, cells subjected to a 3-min OGD or exposed to the medium from cells that had a 3-min OGD were harvested at 30 min after the OGD or the medium exposure for Western blotting of Akt, a prosurvival protein. Our study showed that a prior episode of ischemia lasting from 3 to 10 min significantly reduced the 1-h OGD-induced cell injury. Medium from cells subjected to a 3-min OGD also induced acute and delayed phases of neuroprotection in OGD-naive human neuron-like cells and primary rat cortical neuronal cultures. Cells subjected to a 3-min OGD or incubated with the medium from cells exposed to a 3-min OGD had increased phosphorylated/activated Akt. The increased phosphorylated Ala and neuroprotection induced by medium transferring were inhibited by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine A1 receptor inhibitor. The 3-min OGD-induced neuroprotection was inhibited by LY294002, an Akt activation inhibitor. These results suggest that ischemic preconditioning-induced neuroprotection is transferable among the cells. Small molecules, such as adenosine, may mediate this effect. (C) 2014 Elsevier Inc. All rights reserved.
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