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Prolonged Alzheimer-like Tau Hyperphosphorylation Induced by Simultaneous Inhibition of Phosphoinositol-3 Kinase and Protein Kinase C in n2a cells

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Acta Biochimica et Biophysica Sinica 2005年第5期37卷 349-354页

作者： Guo-Gang XU Yan-Qiu DEnG Shi-Jie LIU Hong-Lian LI Jian-Zhi WAnG Department of Pothophysiology,Institute of neuroscience,Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China Department of Pathophysiology Institute of Neuroscience Tongji Medical College Huazhong University of Science and TechnologyWuhan 430030 China

Co-injection of wortmannin（inhibitor of phosphatidylinositol-3 kinase,PI3K）and GF109203X（inhibitor of protein kinase C,PKC）into the rat brain was found to induce spatial memory deficiency andenhance tau hyperphosphorylation in the hippocampus of rat *** establish a cell model with durativeAlzheimer-like tau hyperphosphorylation in this study,we treated n2a neuroblastoma cells with wortmanninand GF109203X separately and simultaneously,and measured the glycogen synthase kinase 3（GSK-3）activity by γ-（32）P-labeling and the level of tau phosphorylation by Western *** was found that theapplication of wortmannin alone only transitorily increased the activity of GSK-3（about 1 h）and the level oftau hyperphosphorylation at Ser396/Ser404 and Ser199/Ser202 sites（no longer than 3 h）;however,a prolongedand intense activation of GSK-3（over 12 h）and enhanced tan hyperphosphorylation（about 24 h）wereobserved when these two selective kinase inhibitors were applied *** conclude that the simultaneousinhibition of PI3K and PKC can induce GSK-3 overactivation,and further strengthen and prolong the Alzheimer-like tau hyperphosphorylation in n2a cells,suggesting the establishment of a cell model with early pathologicalevents of Alzheimer’s disease.

关键词： Alzheimer’s disease(AD) tau glycogen synthase kinase 3(GSK-3) protein kinase C(PKC) phosphatidylinositol-3 kinase(PI3K) n2a cells

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Effects of nifedipine on outward Kv currents in n2a cells

Effects of nifedipine on outward Kv currents in N2A cells

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者： Xiantao Li Ximu Hu Xiaoqing Li Xiaoyue Qiu Pengfei Ma Kai Li 中南民族大学生命科学学院

It is well known that nifedipine inhibits L-type Ca2+channels expressed throughout the cardiovascular ***-dependent K+（Kv）channels belong to the same supergene family as Ca2+and na+channels;therefore,these channels could be one of the targets of *** studies suggested that there existed macroscopic Kv currents in mouse neuroblastoma n2a *** the study here,whole-cell recording was performed to examine the actions of nifedipine on outward Kv currents in n2a *** to nifedipine,in a concentration-dependent manner,potently reduced the peak and steady-state currents through Kv *** depression in both the amplitude and the decay rate of Kv currents,with an increase in depolarization,suggested that it was a voltage-dependent *** activation and inactivation experiments were conducted to determine the exact causes of the inhibitory *** to nifedipine did not affect the half-maximum activation potential（V1/2）.For steady-state inactivation,the half-maximum inactivation potential（V1/2）was–45.0 m V and shifted right to–32.5 m V with a statistical difference and the time constants of recovery from inactivation were also altered by nifedipine,suggesting that the depression was correlated with the inactivation gate.

关键词： nifedipine n2a cells Kv currents

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Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis

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neural Regeneration Research 2016年第5期11卷 823-828页

作者： Wei Gao Shu-rui Chen Meng-yao Wu Kai Gao Yuan-long Li Hong-yu Wang Chen-yuan Li Hong Li Department of Biochemistry Liaoning Medical University

Methylprednisolone markedly reduces autophagy and apoptosis after secondary spinal cord injury. Here, we investigated whether pretreatment of cells with methylprednisolone would protect neuron-like cells from subsequent oxidative damage via suppression of autophagy and apoptosis. Cultured n2 a cells were pretreated with 10 μM methylprednisolone for 30 minutes, then exposed to 100 μM H2O2 for 24 hours. Inverted phase contrast microscope images, MTT assay, flow cytometry and western blot results showed that, compared to cells exposed to 100 μM H2O2 alone, cells pretreated with methylprednisolone had a significantly lower percentage of apoptotic cells, maintained a healthy morphology, and showed downregulation of autophagic protein light chain 3B and Beclin-1 protein expression. These findings indicate that methylprednisolone exerted neuroprotective effects against oxidative damage by suppressing autophagy and apoptosis.

关键词： nerve regeneration spinal cord injury methylprednisolone oxidative stress n2a cells autophagy light chain 3B Beclin-1 apoptosis neuroprotection H2O2 neural regeneration

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