The expression pattern of Nischarin after lipopolysaccharides (LPS)-induced neuroinflammation in rats brain cortex
The expression pattern of Nischarin after lipopolysaccharides (LPS)-induced neuroinflammation in rats brain cortex
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DOI：
10.1007/s00011-013-0631-2
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发表时间：
2013-09
影响因子：
6.7
通讯作者：
Xiaohong Wu;Wei Xu;Gang Cui;Yaohua Yan;Xinmin Wu;Lei Li;Xiang-Ling Tan;Qiyun Wu;X. Gu
中科院分区：
文献类型：
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作者：
Xiaohong Wu;Wei Xu;Gang Cui;Yaohua Yan;Xinmin Wu;Lei Li;Xiang-Ling Tan;Qiyun Wu;X. Gu
目的探讨Nischarin是否通过磷脂酰肌醇3激酶（PI 3 K）和蛋白激酶B（PKB）途径参与炎症诱导的神经元凋亡。治疗组大鼠侧脑室注射脂多糖（LPS）。用LPS处理BV-2细胞。方法采用Western blotting方法检测Nischarin、pAKT、BAD和Bcl-2在PC 12细胞中的表达水平。免疫组织化学和免疫荧光法观察Nischarin的形态和定位。结果LPS刺激后Nischarin的表达水平升高，同时Nischarin定位于神经元内。结论Nischarin可能参与了PI 3 K/PKB通路依赖的神经元凋亡过程。结果表明，siRNA沉默Nischarin后，PC 12细胞pAKT和Bcl-2蛋白表达降低，BAD和caspase-3活性增加。
ObjectiveTo investigate whether Nischarin participated in neuronal apoptosis induced by neuroinflammation and via the phosphatidylinositol 3-kinase (PI3K) and PKB-dependent pathway.MaterialUse of male Sprague–Dawley rats, rat pheochromocytoma (PC12), and murine microglial cells (BV-2). Treatment lipopolysaccharides (LPS) were injected into the brain lateral ventricle of the rat. The BV-2 cells were treated by LPS. The PC12 cells were pretreated by or not pretreated by conditioned media and siRNA.MethodsWestern blotting was used for analyzing the expression level of Nischarin, pAKT, BAD and Bcl-2. Immunohistochemistry and immunofluorescence were used to perform the morphology and localization of Nischarin. The siRNA could down-regulate the protein level of endogenous Nischarin.ResultsThe expression level of Nischarin was elevated after LPS injection; meanwhile, Nischarin was located in the neuron. Nischarin was involved in regulating the PI3K/PKB patway.ConclusionNischarin might be involved in mediating the process of PI3K/PKB pathway-dependent neuronal apoptosis. After the silencing of Nischarin in cultured PC12 (pheochromocytoma) by siRNA, these results showed that it would induce a reduction of pAKT and Bcl-2 proteins expression; meanwhile, it induces an increase of BAD and active caspase-3.