机构地区:[1]牡丹江医学院红旗医院药剂科,黑龙江牡丹江157011 [2]牡丹江医学院红旗医院神经内科,黑龙江牡丹江157011
出 处:《中外医疗》2017年第3期28-31,共4页China & Foreign Medical Treatment
基 金:黄芪多糖对脑缺血再灌注后TLR4/MyD88信号通路的影响;牡丹江医学院科学技术研究项目(2011-19)
摘 要:目的研究黄芪和三七成分结合对脑缺血/再灌注小鼠Nα,NF-κB信号通路和炎性因子的影响作用。方法该次研究地点为牡丹江医学院红旗医院药剂科,2016年2—10月选取SP大鼠45只分为假手术组、脑缺血再灌注组、黄芪多糖治疗脑缺血再灌注组,每组15只,其中假手术组只进行大脑中动脉的剥离不进行栓塞。脑缺血再灌注组、黄芪多糖治疗脑缺血再灌注组进行线栓法阻塞大脑中动脉2 h后放开模拟脑缺血再灌注的条件。进行各时间点缺血再灌注后3、6、24、72 h的各个指标的变化。结果脑缺血/再灌注后,脑组织TNF-α、IL-β和ICAM-1m RNA的表达增加,分别为(3.58±0.19)、(1.06±0.18)、(2.39±0.27)。黄芪可以降低TNF-αm RNA的表达(2.58±0.16),三七可以同时降低TNF-α、IL-β和ICAM-1m RNA的表达,分别为(0.65±0.11)、(1.79±0.23)。两种药物的配伍可以显著抑制炎性细胞因子的表达效果。脑缺血/再灌注后,胞质NF-κB蛋白表达显著减少,胞核NF-κB蛋白表达增加,NF-κB的核转为率升高。结论黄芪和三七的主要成分配伍可以有效抑制缺血/再灌注后的脑组织NF-κB信号通路的激活,进而减少炎性细胞因子的生成,进而减轻脑缺血后脑组织继发炎症,更好的保护脑组织。Objective To re se a rch th e effect of as trag alu s mem b rana ceus an d sanqi component on th e N F - kB signal c h a n -nel and inflammatory factor of cerebral ischemia- reperfusion mice. Methods 45 SP rats in d ep a r tm en t of pharmacy,HongqiHospital of Mudanj iang Medical Colkge from February to October 2016 were selected and divided into three groups with 15c a se s in e a ch , th e Sham -o p e ra te d group were given only b ra in a r te r ia l d is se c t io n b u t not embolism, and th e c e re b ra l is ch em ia - re p e r fu s io n group an d th e a s trag a l in tre a tm en t for c e re b ra l is c h em ia - re p e r fu s io n group re le a sed th e condi tion of s tim u la tin g c e re b ra l isch em ia repe rfus io n af te r b locking th e b ra in a r te ry by th e su tu re -o c c lu d e d method, an d th echanges of various indexes at 3,6,24,72 h af ter the ischemia- reperfusion at each time point were observed. Results After the cerebral ischemia- reperfusion,the brain t issue TNF-a, IL-茁 an d ICAM-1mRNA exp res sion could in c re a se , (3 .5 8±0 .1 9), (1.06±0.18), (2 .3 9±0 .2 7 ),an d Astragalus memb rana ceus could re d u c e th e ex p res sion of TNF-amRNA, (2.5 8±0 .1 6) an d San- qi could reduce the expres sion of TNF-a,rL-茁 and ICAM-1m RNA (0.6 5±0 .1 1) and (1.79±0.23) , an d th e comb in ation of th e two drugs could obviously inhibi t the expres sion effect of inflammatory cytokines , af ter cerebral ischemia- reperfusion, the expres sion of kytoplasm NF-kB p ro tein obviously d e c re a se d , and th e ex pression of karyon NF-kB p ro te in obviously in -creased and the examination and transmiss ion rate of NF-kB in c re a se d . Conclusion The comp atibi lity of as trag alu s mem- branaceus and sanqi can effectively inhibi t the activation of brain t issue NF-kB signal ch a n n e l af te r th e
关 键 词:黄芪 三七 脑缺血/再灌注 小鼠NF-κB信号通路 炎性因子
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