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SalvinorinA对原代培养的大鼠皮层神经元缺氧无糖损伤的保护作用及其机制研究
The neuroprotective effects and mechanisms of Salvinorin A on the injury of oxygen-glucose deprivation in primary cultured cortical neurons of rats

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DOI:
作者:
吴广喜，黄莉莉，张骁，焦英甫，贺平，苏殿三
WU Guangxi,HUANG Lili,ZHANG Xiao,JIAO Yingfu,HE Ping,SU Diansan
作者单位:
上海交通大学医学院附属仁济医院麻醉科
Department of Anesthesiology，Renji Hospital, School of Medicine,Shanghai Jiaotong University
关键词:
Salvinorin A；氧糖剥夺；神经保护
Salvinorin A；oxygen-glucose deprivation；neuroprotection
摘要:
目的 研究Salvinorin A对原代培养的大鼠皮层神经元缺氧无糖损伤的保护作用，并研究其可能的机制。方法 原代培养大鼠皮层神经元，并建立氧糖剥夺模型。然后观察不同剂量Salvinorin A对于神经元氧糖剥夺损伤是否具有保护作用，并选择最佳剂量进行后续的研究。然后应用MAPK通路的三种不同的抑制剂，分别是ERK通路抑制剂U0126，P38通路的抑制剂SB200235和JNK通路的抑制剂SP600125，观察Salvinorin A 保护作用的变化，最终证明其作用机制。结果 原代培养的大鼠皮层神经元在缺氧无糖的损伤下，乳酸脱氢酶的漏出率明显增加。Salvinorin A 对该损伤表现出了明显的剂量依赖性，其中1μM浓度的Salvinorin A是具有明显保护作用的最低剂量。三种抑制剂中只有ERK通路的抑制剂U0126能够明显逆转Salvinorin A 的保护作用，说明其保护作用的机制是通过ERK通路实现的。结论 Salvinorin A能够剂量依赖性的保护原代培养的大鼠皮层神经元的氧糖剥夺损伤，其机制与ERK通路相关。
Objective： To observe the neuroprotective effects and mechanisms of Salvinorin A on the injury of oxygen-glucose deprivation in primary cultured cortical neurons of rats. Methods： Primary rat cortex neurons were cultured and then oxygen-glucose deprivation(OGD) was performed. Then the neuroprotective effects of different doses of Salvinorin A were tested by measuring the release rate of lactate dehydrogenase（LDH）. The optimal dose was selected for following studys. In order to investigate the mechanisms of Salvinorin A, three inhibitors of MAPK pathways, ERK pathway inhibitor U0126, P38 pathway inhibitor SB200235 and JNK pathway inhibitor SP600125, were added and the neuroprotective effects were tested again. Results： The release rate of LDH of primary rat cortical neurons after oxygen-glucose deprivation was obviously increased compared with the control group. Salvinorin A showed obvious dose-dependent protective effects to the injury. And 1 μM Salvinorin A was selected as the optimal dose because it is the lowest dose with obvious protective effect. Moreover, only the ERK pathway inhibitor U0126 can reverse the neuroprotective effect of Salvinorin A. Conclusion: Salvinorin A had dose dependently neuroprotective effects on the injury of oxygen-glucose deprivation in primary cultured cortical neurons of rats. ERK/MAPK pathway was involved in the mechanism of the neuroprotective effects of Salvinorin A.

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