利用知识发现工具Arrowsmith探讨龙血竭及其有效成分治疗缺血性脑卒中的潜在作用机制  

Explore Latent Mechanism of Dracaenea Cochinchinensis Resina in Treating Ischemic Stroke by Using Knowledge-Discovery Tool Arrowsmith

作　　者：王仁杰[1,2] 张艳军 王星星[1,2] 张新庄 周建明[1] 萧伟 WANG Ren-jie ZHANG Yan-jun WANG Xing-xing ZHANG Xin-zhuang ZHOU Jian-ming XIAO Wei(State Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Jiangsu Kanion Pharmaceutical Co. Ltd. , Lianyungang 222001, China Key Laboratory for New Technique Research of TCM Extraction and Purification, Lianyungang 222001, China)

机构地区：[1]江苏康缘药业股份有限公司中药制药过程新技术国家重点实验室,江苏连云港222001 [2]中药提取精制新技术重点研究室,江苏连云港222001

出　　处：《中国实验方剂学杂志》2017年第22期194-201,共8页Chinese Journal of Experimental Traditional Medical Formulae

基　　金：国家"重大新药创制"科技重大专项(2013ZX09402203)

摘　　要：目的:探讨龙血竭治疗缺血性脑卒中的可能机制。方法:运用非相关文献知识发现工具Arrowsmith在线软件,通过分析龙血竭和缺血性脑卒中两个主题词文献集合的中间词,探求潜在机制。结果:Arrowsmith软件的初步探索结果显示龙血竭及其有效成分对环氧合酶-2(cyclooxygenase-2,COX-2),瞬时感受器电位香草酸受体1(transient receptor potential vanilloid 1,TRPV_1),一氧化氮合酶(nitric oxide synthase,NOS),电压门控性钾通道1.3(voltage-gated potassium channel 1.3,Kv1.3)及转化生长因子-β_1(transforming growth factor-β_1,TGF-β_1)具有调节作用,同时在缺血性脑卒中过程中上述指标也出现异常表达。结论:龙血竭治疗缺血性脑卒中的机制可能与下调缺血性脑组织中COX-2和诱导型一氧化氮合酶(i NOS)的表达、拮抗TRPV_1和Kv1.3通道、上调内皮型一氧化氮合酶(e NOS)和TGF-β_1的表达有关,可为进一步开展机制验证性研究提供参考。Objective： To explore the potential mechanism of Dracaenea Cochinchinensis Resina in the treatment of ischemic stroke. Method： Online software of Arrowsmith based on the theory of Swanson＇s noncorrelated literature-bases knowledge discovery was applied to explore the underlying mechanism by analyzing the intermediate words in the literature on Dracaenea Cochinchinensis Resina and ischemic stroke. Result： The preliminary investigation results by Arrowsmith software showed that Dracaenea Cochinchinensis Resina and its active components might have certain ability to regulate the expression levels of cyclooxygenase-2（ COX-2）,transient receptor potential vanilloid 1（ TRPV1）,nitric oxide synthase（ NOS）,voltage-gated potassium channel1. 3（ Kv1. 3） and transforming growth factor-β1（ TGF-β1）; and these above indexes had abnormal expression in ischemic stroke. Conclusion： The mechanism may be associated with down-regulating the expression of COX-2 and i NOS,blocking TRPV1 and Kv1. 3 channel,and promoting the expression of e NOS and TGF-β1. This can provide strong reference for the laboratory to conduct further mechanism verification studies.

关 键 词：龙血竭 缺血性脑卒中 Arrowsmith 环氧合酶-2 瞬时感受器电位香草酸受体1 一氧化氮合酶 电压门控性钾通道1.3 转化生长因子-Β1 

分 类 号：R287[医药卫生—中药学] R285.5[医药卫生—中医学]