阿立哌唑对Aβ25-35诱导的神经PC12细胞损伤的影响及机制-中国药房

阿立哌唑对Aβ25-35诱导的神经PC12细胞损伤的影响及机制

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篇名：	阿立哌唑对Aβ25-35诱导的神经PC12细胞损伤的影响及机制
TITLE：
摘要：	目的：研究阿立哌唑对Aβ淀粉样蛋白（Aβ25-35）诱导的神经PC12细胞损伤的影响及其机制。方法：将PC12细胞随机分为正常对照组、模型组（20 μmol/L Aβ25-35）和阿立哌唑低、中、高浓度组（5、10、20 μmol/L阿立哌唑+20 μmol/L Aβ25-35），加入含相应药物的培养基培养48 h，每组6个复孔。MTT法检测细胞活力（光密度值），Hoechst染色法检测细胞凋亡情况，分光光度法检测细胞中天冬氨酸特异性蛋白酶3（Caspase-3）、Caspase-9活性，Western blot法检测细胞中B淋巴细胞瘤2（Bcl-2）、Bcl-2相关X蛋白（Bax）、磷脂酰肌醇3 激酶（PI3K）蛋白表达及蛋白激酶B（Akt）磷酸化水平。结果：与正常对照组比较，模型组细胞光密度值降低，凋亡率增加，Caspase-3、Caspase-9活性和Bax蛋白表达均增强，Bcl-2、PI3K蛋白表达和Akt磷酸化水平均降低（P＜0.01）。与模型组比较，阿立哌唑低、中、高浓度组细胞光密度值增加，凋亡率减少，Caspase-3、Caspase-9活性减弱，Bcl-2、PI3K蛋白表达和Akt磷酸化水平均增加；阿立哌唑中、高浓度组细胞Bax蛋白表达减弱（P＜0.05或P＜0.01）。结论：阿立哌唑可明显抑制Aβ25-35诱导的PC12细胞凋亡，其作用可能与激活PI3K/Akt信号通路有关。
ABSTRACT：	OBJECTIVE： To study the effects of aripiprazole on PC12 cell injury induced by amyloid β-protein （Aβ25-35） and its mechanism. METHODS： PC12 cells were randomized into normal control group， model group （20 μmol/L Aβ25-35）， aripiprazole low-concentration， medium-concentration and high-concentration groups （5， 10， 20 μmol/L aripiprazole+20 μmol/L Aβ25-35）. These groups were cultured with culture medium containing relevant medicine for 48 h， with 6 wells in each group. The viability （optical density value） of PC12 cell was measured by MTT assay， and PC12 cell apoptosis was measured by Hoechst staining. The activities of Caspase-3 and Caspase-9 were determined by spectrophotometry. The protein expression of Bcl-2， Bax and PI3K and the phosphorylation of Akt were assayed by Western blot assay. RESULTS： Compared with normal control group， optical density value of model group was decreased while apoptotic rate was increased； the activities of Caspase-3 and Caspase-9， and the protein expression of Bax were increased； the protein expression of Bcl-2 and PI3K， the phosphorylation of Akt were decreased （P＜0.01）. Compared with model group， optical density value of aripiprazole low-concentration， medium-concentration and high-concentration groups were increased， while apoptotic rate and the activities of Caspase-3 and Caspase-9 were decreased； the protein expression of Bcl-2 and PI3K and the phosphorylation of Akt were enhanced； while the protein expression of Bax were decreased in aripiprazole medium-concentration and high-concentration groups （P＜0.05 or P＜0.01）. CONCLUSIONS： Aripiprazole can suppress cell apoptosis of PC12 cell induced by Aβ25-35， which is related to activating PI3K/Akt signal pathway.
期刊：	2017年第28卷第1期
作者：	杨淑珍，赵晶媛
AUTHORS：	YANG Shuzhen，ZHAO Jingyuan
关键字：	阿立哌唑；Aβ淀粉样蛋白；神经PC12细胞；凋亡；磷脂酰肌醇3 激酶/蛋白激酶B信号通路
KEYWORDS：	Aripiprazole； Amyloid β-protein； Nerve PC12 cell； Apoptosis； PI3K/Akt signal pathway
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