Nao-Fu-Cong ameliorates diabetic cognitive dysfunction by inhibition of JNK/CHOP/Bcl2-mediated apoptosis in vivo and in vitro

作     者：JING Guang-Chan LIU Di LIU Yu-Qin ZHANG Meng Ren JING Guang-Chan;LIU Di;LIU Yu-Qin;ZHANG Meng-Ren

作者机构：Deparment of Traditional Chinese MedicinePeking Union Medical Collge HospitalPeking Union Medical Collge and Chinese Academy of Medical SciencesBeijing 100730China Deparment 0f cell resource centerInstitute of Basic Medical SciencePeking Union Medical College and Chinese Academy of Medical SciencesBeijing 100730China 

出 版 物：《Chinese Journal of Natural Medicines》 (中国天然药物（英文版）)

年 卷 期：2020年第18卷第9期

页      面：704-713页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 100602[医学-中西医结合临床] 10[医学] 

基　　金：supported by the Beijing Natural Science Foundation (No. 7142129) 

主　　题：Nao-Fu-Cong Apoptosis High glucose Hippocampal neurons 

摘      要：Chinese herbal compound Nao-Fu-Cong(NFC) has been mainly used to treat cognitive disorders in Traditional Chinese Medicine(TCM). The present study aimed to investigate whether its neuroprotective effects might be related to the inhibition of JNK/CHOP/Bcl2-mediated apoptosis pathway or not. We randomly assigned STZ(60 mg·k^(-1))-induced diabetic rats into control group, diabetic model group and NFC groups(low-dose, medium-dose and high-dose). The primary culture of hippocampal neurons were transferred into different culture media on the third day. The cells were then divided into control group, high-glucose group, NFC(low-dose, medium-dose and high-dose) groups, CHOP si-RNA intervention group, JNK pathway inhibitor SP600125 group and oxidative stress inhibitor N-acetylcysteine(NAC) group. NFC significantly improved the cognitive function of diabetic rats, and had neuroprotective effect on hippocampal neurons cultured in high glucose. Further research results showed that NFC could reduce the apoptosis of hippocampal neurons in rats with diabetic cognitive dysfunction. NFC had inhibitory effects on CHOP/JNK apoptosis pathway induced by high glucose, and also decreased the levels of ROS and increased the mitochondrial membrane potential. These suggested that the neuroprotective effect of NFC might be related to the inhibition of CHOP and JNK apoptotic signaling pathways, and the cross pathway between oxidative stress and mitochondrial damage pathway.