Schizandrin protects primary rat cortical cell cultures from glutamate-induced apoptosis by inhibiting activation of the MAPK family and the mitochondria dependent pathway.
Schizandrin protects primary rat cortical cell cultures from glutamate-induced apoptosis by inhibiting activation of the MAPK family and the mitochondria dependent pathway.
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精神分裂素通过抑制MAPK家族的激活和线粒体依赖性途径来保护原发性大鼠皮质细胞培养物免受谷氨酸诱导的凋亡。
DOI：
10.3390/molecules18010354
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发表时间：
2012-12-27
期刊：
影响因子：
--
通讯作者：
Cheng HY
中科院分区：
文献类型：
--
作者：
Lee MS;Chao J;Yen JC;Lin LW;Tsai FS;Hsieh MT;Peng WH;Cheng HY
谷氨酸诱导的兴奋性毒性与多种神经元退行性疾病有关。在本研究中，我们研究了五味子甲素对谷氨酸诱导的原代培养大鼠皮质细胞凋亡的可能的神经保护作用。施用谷氨酸（10 μM）24小时可降低Bcl-2和Bcl-XL蛋白的表达，而增加Bax、Bak、凋亡诱导因子（AIF）、内切核酸酶G（Nodo G）和caspase-12的内质网（ER）应激的表达。与仅用谷氨酸处理相比，在谷氨酸处理之前用五味子甲素 (100 μM) 预处理可增加 Bcl-XL 和 Bcl-2 的表达，并减少 Bax、Bak、AIF、Nodo G 和 caspase-12 的表达。此外，谷氨酸诱导 JNK、p38 和 ERK 丝裂原激活蛋白激酶 (MAPK) 磷酸化，而这些作用可通过五味子素 (100 μM) 处理减弱。这些结果表明五味子甲素具有神经保护作用。五味子素抗谷氨酸诱导的细胞凋亡的分子机制可能涉及调节Bcl-2家族蛋白的表达，以及通过阻断JNK、ERK和p38 MAPK的激活来调节内质网应激。
Glutamate-induced excitotoxicity has been implicated in a variety of neuronal degenerative disorders. In the present study, we investigated the possible neuroprotective effects of schizandrin against apoptosis of primary cultured rat cortical cells induced by glutamate. Glutamate (10 μM) administered for 24 h decreased the expression of Bcl-2 and Bcl-XL protein, whereas increased the expression of Bax, Bak, apoptosis inducing factor (AIF), endonuclease G (Nodo G) and endoplasmic reticulum (ER) stress of caspase-12. Pretreatment with schizandrin (100 μM) before glutamate treatment increased the Bcl-XL and Bcl-2 expression and decreased Bax, Bak, AIF, Nodo G and caspase-12 compared with those only treated with glutamate. Furthermore, glutamate-induced phosphorylation of JNK, p38 and ERK mitogen-activated protein kinases (MAPK), and these effects were attenuated by schizandrin (100 μM) treatment. These results suggest that schizandrin possesses the neuroprotective effects. The molecular mechanisms of schizandrin against glutamate-induced apoptosis may involve the regulation of Bcl-2 family proteins expression, and ER stress through blocking the activation of JNK, ERK and p38 MAPK.
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