中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2014年
9期
1005-1009
,共5页
脑梗死%缺血预处理%成体干细胞%受体,阿片样,S%皂苷类
腦梗死%缺血預處理%成體榦細胞%受體,阿片樣,S%皂苷類
뇌경사%결혈예처리%성체간세포%수체,아편양,S%조감류
Brain infarction%Ischemic preconditioning%Adult stem cells%Receptors,opioid,delta%Saponins
目的 明确缺血预处理(IPC)及中药三七三醇皂苷(PTS)对大鼠脑梗死后7d脑海马区自体神经干细胞增殖、神经行为学评分,以及δ阿片受体(DOR)、Bax和Bcl-2 mRNA表达水平的影响. 方法 采用二次线栓法建立局灶性SD大鼠脑缺血耐受动物模型.80只SD雄性大鼠随机分为:假手术(Sham)组、缺血(MCAO)组、假手术+缺血(Sham+ MCAO)组、预缺血+缺血(IP+MCAO)组、三七三醇皂苷-缺血(PTS+ MCAO)组.每组取10只行BrdU荧光标记细胞免疫组化染色,另6只行荧光定量PCR测定DOR、Bax、Bcl-2 mRNA水平.大鼠在处死前1d予腹腔注射BrdU.采用Zea-Longa评分方法对大鼠脑梗死后7d进行神经行为学评分,运用荧光免疫组织化学技术检测大鼠脑缺血侧海马区BrdU标记阳性细胞数量. 结果 SD大鼠脑梗死后7d,Zea-Longa神经行为学评分MCAO、Sham+ MCAO两组与IP+ MCAO、PTS+ MCAO间均差异有统计学意义(P＜0.01),而MCAO和Sham+ MCAO组间、IP+ MCAO和PTS+ MCAO组间差异无统计学意义(P＞0.05).SD大鼠脑梗死后7d,缺血侧海马区BrdU标记阳性细胞Sham、MCAO、Sham+ MCAO3组与IP+ MCAO、PTS+ MCAO间均有差异(P＜0.01);而MCAO和Sham+MCAO组间、IP+MCAO和PTS+ MCAO组间差异无统计学意义(P＞0.05).IP+ MCAO组,DOR、Bcl-2 mRNA的表达水平明显高于MCAO、Sham+ MCAO和PTS+ MCAO组(P＜0.01),而Bax mRNA的表达水平明显低于MCAO、Sham+ MCAO和PTS+ MCAO组(P＜0.01).MCAO、Sham+ MC AO和PTS+ MCAO3组间差异无统计学意义(P＞0.05). 结论 IPC可促进大鼠脑梗死后海马区成体神经干细胞增殖,并能改善其神经功能缺损症状;IPC可促使DOR、Bcl-2 mRNA水平的上调,并降低BaxmRNA的表达水平;PTS可改善大鼠脑梗死后的神经功能缺损症状,促使大鼠海马齿状回颗粒成体神经干细胞增殖,但对DOR、Bcl-2、Bax mRNA表达水平无影响.
目的 明確缺血預處理(IPC)及中藥三七三醇皂苷(PTS)對大鼠腦梗死後7d腦海馬區自體神經榦細胞增殖、神經行為學評分,以及δ阿片受體(DOR)、Bax和Bcl-2 mRNA錶達水平的影響. 方法 採用二次線栓法建立跼竈性SD大鼠腦缺血耐受動物模型.80隻SD雄性大鼠隨機分為:假手術(Sham)組、缺血(MCAO)組、假手術+缺血(Sham+ MCAO)組、預缺血+缺血(IP+MCAO)組、三七三醇皂苷-缺血(PTS+ MCAO)組.每組取10隻行BrdU熒光標記細胞免疫組化染色,另6隻行熒光定量PCR測定DOR、Bax、Bcl-2 mRNA水平.大鼠在處死前1d予腹腔註射BrdU.採用Zea-Longa評分方法對大鼠腦梗死後7d進行神經行為學評分,運用熒光免疫組織化學技術檢測大鼠腦缺血側海馬區BrdU標記暘性細胞數量. 結果 SD大鼠腦梗死後7d,Zea-Longa神經行為學評分MCAO、Sham+ MCAO兩組與IP+ MCAO、PTS+ MCAO間均差異有統計學意義(P＜0.01),而MCAO和Sham+ MCAO組間、IP+ MCAO和PTS+ MCAO組間差異無統計學意義(P＞0.05).SD大鼠腦梗死後7d,缺血側海馬區BrdU標記暘性細胞Sham、MCAO、Sham+ MCAO3組與IP+ MCAO、PTS+ MCAO間均有差異(P＜0.01);而MCAO和Sham+MCAO組間、IP+MCAO和PTS+ MCAO組間差異無統計學意義(P＞0.05).IP+ MCAO組,DOR、Bcl-2 mRNA的錶達水平明顯高于MCAO、Sham+ MCAO和PTS+ MCAO組(P＜0.01),而Bax mRNA的錶達水平明顯低于MCAO、Sham+ MCAO和PTS+ MCAO組(P＜0.01).MCAO、Sham+ MC AO和PTS+ MCAO3組間差異無統計學意義(P＞0.05). 結論 IPC可促進大鼠腦梗死後海馬區成體神經榦細胞增殖,併能改善其神經功能缺損癥狀;IPC可促使DOR、Bcl-2 mRNA水平的上調,併降低BaxmRNA的錶達水平;PTS可改善大鼠腦梗死後的神經功能缺損癥狀,促使大鼠海馬齒狀迴顆粒成體神經榦細胞增殖,但對DOR、Bcl-2、Bax mRNA錶達水平無影響.
목적 명학결혈예처리(IPC)급중약삼칠삼순조감(PTS)대대서뇌경사후7d뇌해마구자체신경간세포증식、신경행위학평분,이급δ아편수체(DOR)、Bax화Bcl-2 mRNA표체수평적영향. 방법 채용이차선전법건립국조성SD대서뇌결혈내수동물모형.80지SD웅성대서수궤분위:가수술(Sham)조、결혈(MCAO)조、가수술+결혈(Sham+ MCAO)조、예결혈+결혈(IP+MCAO)조、삼칠삼순조감-결혈(PTS+ MCAO)조.매조취10지행BrdU형광표기세포면역조화염색,령6지행형광정량PCR측정DOR、Bax、Bcl-2 mRNA수평.대서재처사전1d여복강주사BrdU.채용Zea-Longa평분방법대대서뇌경사후7d진행신경행위학평분,운용형광면역조직화학기술검측대서뇌결혈측해마구BrdU표기양성세포수량. 결과 SD대서뇌경사후7d,Zea-Longa신경행위학평분MCAO、Sham+ MCAO량조여IP+ MCAO、PTS+ MCAO간균차이유통계학의의(P＜0.01),이MCAO화Sham+ MCAO조간、IP+ MCAO화PTS+ MCAO조간차이무통계학의의(P＞0.05).SD대서뇌경사후7d,결혈측해마구BrdU표기양성세포Sham、MCAO、Sham+ MCAO3조여IP+ MCAO、PTS+ MCAO간균유차이(P＜0.01);이MCAO화Sham+MCAO조간、IP+MCAO화PTS+ MCAO조간차이무통계학의의(P＞0.05).IP+ MCAO조,DOR、Bcl-2 mRNA적표체수평명현고우MCAO、Sham+ MCAO화PTS+ MCAO조(P＜0.01),이Bax mRNA적표체수평명현저우MCAO、Sham+ MCAO화PTS+ MCAO조(P＜0.01).MCAO、Sham+ MC AO화PTS+ MCAO3조간차이무통계학의의(P＞0.05). 결론 IPC가촉진대서뇌경사후해마구성체신경간세포증식,병능개선기신경공능결손증상;IPC가촉사DOR、Bcl-2 mRNA수평적상조,병강저BaxmRNA적표체수평;PTS가개선대서뇌경사후적신경공능결손증상,촉사대서해마치상회과립성체신경간세포증식,단대DOR、Bcl-2、Bax mRNA표체수평무영향.
Objective To investigate the effect of brain ischemic preconditioning (IP) combined with traditional Chinese medicine three seven three alcohol saponin (PTS) on proliferation of endogenous neural stem cells and the mRNA expressions of delta opioid receptor (DOR),Bax,Bcl-2 in hippocampus at 7d post middle cerebral artery occlusion (MCAO).Methods The focal-focal ischemic tolerance models were established with twice suture method.80 SD rats were included and randomly divided into 5 groups:sham group,MCAO group,sham+ MCAO group,IP+ MCAO group,PTS+MCAO group (n=16 each).We chose 10 SD rats from each group to evaluate their neurological status,and made BrdU fluorescent immunolabeling.In addition,we chose the other 6 SD rats to detect the expression levels of DOR,Bax and Bcl-2 mRNA in ischemic region in hippocampusby using RT-PCR.Animals were given one set of BrdU injections (on day 6,three times,4h apart,50mg/kg) to label the proliferating cells.The neurological status was assessed by using Zea Longa neurological deficit scores at 7 days following cerebral infarction.Results Zea longa neurologic deficit scores in MCAO group and sham+ MCAO) group had significantly differences with IP+ MCAO group and PTS+ MCAO group respectively at 7d post MCAO(P＜0.01).There was no significant differeuce in Zea-longa neurologic deficit scores between MCAO group versus sham+ MCAO group,and IP+ MCAO group versus PTS+ MCAO group(P＞0.05).The number of BrdU+ ceils in hippocampus had significant differences between IP+ MCAO and PTS+ MCAO groups at 7d post MCAOand three groups of sham,MCAO and sham+ MCAO respectively (P＜0.01).There was no difference in the number of BrdU+ cells between MCAO versus Sham + MCAO groups and IP + MCAO versus PTS+MCAO groups(P＞0.05).DOR and Bcl-2 mRNA expression levels were higher and Bax mRNA expression level was lower in IP+ MCAO group than in MCAO,Sham+ MCAO and PTS+MCAO groups (P＜0.01).There were no significant differences in DOR,Bcl-2 and Bax mRNA expressions among MCAO,Sham + MCAO and PTS + MCAO groups (P＞ 0.05).Conclusions Acute cerebral infarction can induce the proliferation of endogenous neural stem cells in hippocampus in SD rats.IPC can facilitate the proliferation of endogenous neural stem cells in hippocampus afteracute cerebral infarction,improve the symptoms of neurologic dysfunction,increase DOR and Bcl 2 mRNA expressions,and reduce Bax mRNA expression in SD rats.PTS can facilitate the proliferation of endogenous neural stem cells in hippocampus after acute cerebral infarction in SD rats,and improve the symptoms of neurologic dysfunction,but it has no influence on the expressions of DOR,Bcl-2 and Bax mRNA.
