摘要
PI3K/Akt信号通路激活所介导的具有中枢神经保护作用的中药非常广泛,但主要分布在补益药、清热药及活血药中,其中尤以补益类中药的苷类及多糖类成分、清热类中药的生物碱类成分为目前研究的热点。基于PI3K/Akt信号通路的中药及其活性成分的中枢神经保护作用作用研究,为相关中枢神经保护剂及PI3K/Akt通路激活剂的开发提供了进一步的实验依据,对神经系统功能障碍性疾病新的、安全的治疗方案与思路开发具有广阔的前景。但目前多数研究对PI3K/Akt通路的下游信号蛋白如Bcl-2,Bax,p21,p-mTOR,p53,Caspase-9,e NOS等关注较多,而对上游蛋白仅对PI3K,Akt,c AMP,PKA,p-PDK等有所研究,对有效部位或有效部位群等中药提取物作为PI3K/Akt信号通路激活剂来保护中枢神经的相关研究较少。
The traditional Chinese medicine( TCMs) mediated by activation of PI3K/Akt signaling pathway for central neuroprotective effects were very extensive,but mainly distributed in TCMs for invigoration,heat-clearing,detoxicating and activating blood circulation. The current research focused on glycosides and polysaccharides from TCMs for invigoration and alkaloids from TCMs for heat-clearing and detoxicating. Central neuroprotective effects of TCMs and its active constituents based on PI3K/Akt signaling pathway can provide further experimental evidence for development of relevant central neuroprotective agents and PI3K/Akt pathway activators,and have broad prospects for development of new and safe treatment options and ideas for neurological dysfunctions.Most studies focused on the downstream signaling proteins such as Bcl-2,Bax,p21,p-mTOR,p53,Caspase-9,eNOS,etc. For upstream signaling proteins,only PI3K,Akt,cAMP,PKA,and p-PDK have been studied. Few studies have investigated effective parts extracted from TCMs mediated by activation of PI3K/Akt signaling pathway to protect central nervous.
作者
顾志荣
许爱霞
李芳
祁梅
马天翔
葛斌
GU Zhi-rong;XU Ai-xia;LI Fang;QI Mei;MA Tian-xiang;GE Bin(Department of Pharmacy,Gansu Provincial People's Hospital,Lanzhou 730000 ,China;Gansu University of Traditional Chinese Medicine,Lanzhou 730000 ,China)
出处
《中国新药杂志》
CAS
CSCD
北大核心
2019年第13期1593-1599,共7页
Chinese Journal of New Drugs
基金
国家自然科学基金(81260597)
甘肃省中医方药挖掘与创新转化重点实验室/甘肃省中药新产品创制省级工程实验室开放课题(ZYFYZH-KJ-2016-005)
甘肃省人民医院青年科研项目(16GSSY7-2)
甘肃省人民医院研发攻关项目(18GSSY2-3)
关键词
中药
活性成分
磷脂酰肌醇3-激酶
蛋白激酶B
信号通路
中枢神经保护作用
TCMs
active constituents
phosphatidylinositol-3-kinase
protein kinase B
signaling pathway
central neuroprotective effect