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Intervention Timing and Effect of PJ34 on astrocytes During Oxygen-glucose Deprivation/reperfusion and Cell Death Pathways

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2015年第3期35卷 397-404页

作者：蔡川张睿黄巧英曹旭邹良玉褚晓凡 Department of Neurology Second Clinical College Jinan University Research Centre for Neural Engineering Institute of Biomedical and Health Engineering Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences

Poly （ADP-ribose） polymerase-I （PARP-1） plays as a double edged sword in cerebral ischemia-reperfusion, hinging on its effect on the intracellular energy storage and injury severity, and the prognosis has relationship with intervention timing. During ischemia injury, apoptosis and oncosis are the two main cell death pathway sin the ischemic core. The participation of astrocytes in ische- mia-reperfusion induced cell death has triggered more and more attention. Here, we examined the pro- tective effects and intervention timing of the PARP-1 inhibitor PJ34, by using a mixed oxygen-glucose deprivation/reperfusion （OGDR） model of primary rat astrocytes in vitro, which could mimic the ische- mia-reperfusion damage in the ＂ischemic core＂. Meanwhile, cell death pathways of various P J34 treated astrocytes were also investigated. Our results showed that P J34 incubation （10 μmol/L） did not affect release of lactate dehydrogenase （LDH） from astrocytes and cell viability or survival 1 h after OGDR. Interestingly, after 3 or 5 h OGDR, P J34 significantly reduced LDH release and percentage of PI-positive cells and increased cell viability, and simultaneously increased the caspase-dependent apop- totic rate. The intervention timing study demonstrated that an earlier and longer P J34 intervention dur- ing reperfusion was associated with more apparent protective effects. In conclusion, earlier and longer PJ34 intervention provides remarkable protective effects for astrocytes in the ＂ischaemic core＂ mainly by reducing oncosis of the astrocytes, especially following serious OGDR damage.

关键词： PARP-1 inhibitor PJ34 primarycortical astrocyte oxygen-glucose deprivation/reperfusion oncosis apoptosis

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