医学临床研究
醫學臨床研究
의학림상연구
JOURNAL OF CLINICAL RESEARCH
2015年
5期
948-950,951
,共4页
丹参/治疗应用%红花/治疗应用%注射剂%脑缺血/代谢%再灌注损伤%HSP20热休克蛋白质类%大鼠 ,Sprague-Dawley
丹參/治療應用%紅花/治療應用%註射劑%腦缺血/代謝%再灌註損傷%HSP20熱休剋蛋白質類%大鼠 ,Sprague-Dawley
단삼/치료응용%홍화/치료응용%주사제%뇌결혈/대사%재관주손상%HSP20열휴극단백질류%대서 ,Sprague-Dawley
Salvia miltiorrhiza/TU%Carthamus tinctorius/TU%INJECTIO%Brain Ischemia/ME%Reperfusion Injury%HSP20 Heat-Shock Proteins%Rats,Sprague-Dawley
【目的】探讨丹红注射液干预大鼠脑缺血再灌注损伤后热休克蛋白(Hsp )20表达及意义。【方法】104只SD大鼠随机分为:8只正常对照(C组),未做任何处理;缺血再灌注损伤48只(I/R组),丹红注射液干预48只(DI/R组)。I/R组与DI/R组均采用大脑中动脉闭塞方法制作大鼠脑缺血再灌注模型,DI/R组从实验前一天开始腹腔注射丹红注射液(8 mL/kg ,Qd),直到各时间点(脑缺血2h再灌注后6h、24h、48h、72h、7d,每个时间点8只)处死,I/R组与DI/R组相同时间点注射生理盐水。比较I/R组与DI/R组脑梗死体积和各时间点神经功能缺损评分和 Hsp20阳性细胞数。【结果】I/R组脑梗死体积为(105.11±10.60)mm3,显著高于DI/R组(82.16±7.02)mm3,其差异有统计学意义( P <0.05)。I/R组脑缺血再灌注后6 h神经功能缺损评分与DI/R组比较无显著性差异(P>0.05),而在24h、48h、72h、7d时,I/R组的神经功能缺损评分显著高于DI/R组(P<0.05),DI/R组缺血再灌注时间越长,神经功能缺损评分越低。正常对照组神经细胞中Hsp20阳性细胞很少;I/R组 Hsp20的表达6 h开始随时间增加,在72 h Hsp20表达达到高峰,7 d表达陡然减少;DI/R组 Hsp20阳性细胞数趋势同I/R组,且均显著高于I/R组相应的各时间点阳性细胞数( P <0.05)。【结论】大鼠脑缺血再灌注损伤后丹红干预,其大鼠Hsp20的表达增加,脑缺血后损伤程度减轻。
【目的】探討丹紅註射液榦預大鼠腦缺血再灌註損傷後熱休剋蛋白(Hsp )20錶達及意義。【方法】104隻SD大鼠隨機分為:8隻正常對照(C組),未做任何處理;缺血再灌註損傷48隻(I/R組),丹紅註射液榦預48隻(DI/R組)。I/R組與DI/R組均採用大腦中動脈閉塞方法製作大鼠腦缺血再灌註模型,DI/R組從實驗前一天開始腹腔註射丹紅註射液(8 mL/kg ,Qd),直到各時間點(腦缺血2h再灌註後6h、24h、48h、72h、7d,每箇時間點8隻)處死,I/R組與DI/R組相同時間點註射生理鹽水。比較I/R組與DI/R組腦梗死體積和各時間點神經功能缺損評分和 Hsp20暘性細胞數。【結果】I/R組腦梗死體積為(105.11±10.60)mm3,顯著高于DI/R組(82.16±7.02)mm3,其差異有統計學意義( P <0.05)。I/R組腦缺血再灌註後6 h神經功能缺損評分與DI/R組比較無顯著性差異(P>0.05),而在24h、48h、72h、7d時,I/R組的神經功能缺損評分顯著高于DI/R組(P<0.05),DI/R組缺血再灌註時間越長,神經功能缺損評分越低。正常對照組神經細胞中Hsp20暘性細胞很少;I/R組 Hsp20的錶達6 h開始隨時間增加,在72 h Hsp20錶達達到高峰,7 d錶達陡然減少;DI/R組 Hsp20暘性細胞數趨勢同I/R組,且均顯著高于I/R組相應的各時間點暘性細胞數( P <0.05)。【結論】大鼠腦缺血再灌註損傷後丹紅榦預,其大鼠Hsp20的錶達增加,腦缺血後損傷程度減輕。
【목적】탐토단홍주사액간예대서뇌결혈재관주손상후열휴극단백(Hsp )20표체급의의。【방법】104지SD대서수궤분위:8지정상대조(C조),미주임하처리;결혈재관주손상48지(I/R조),단홍주사액간예48지(DI/R조)。I/R조여DI/R조균채용대뇌중동맥폐새방법제작대서뇌결혈재관주모형,DI/R조종실험전일천개시복강주사단홍주사액(8 mL/kg ,Qd),직도각시간점(뇌결혈2h재관주후6h、24h、48h、72h、7d,매개시간점8지)처사,I/R조여DI/R조상동시간점주사생리염수。비교I/R조여DI/R조뇌경사체적화각시간점신경공능결손평분화 Hsp20양성세포수。【결과】I/R조뇌경사체적위(105.11±10.60)mm3,현저고우DI/R조(82.16±7.02)mm3,기차이유통계학의의( P <0.05)。I/R조뇌결혈재관주후6 h신경공능결손평분여DI/R조비교무현저성차이(P>0.05),이재24h、48h、72h、7d시,I/R조적신경공능결손평분현저고우DI/R조(P<0.05),DI/R조결혈재관주시간월장,신경공능결손평분월저。정상대조조신경세포중Hsp20양성세포흔소;I/R조 Hsp20적표체6 h개시수시간증가,재72 h Hsp20표체체도고봉,7 d표체두연감소;DI/R조 Hsp20양성세포수추세동I/R조,차균현저고우I/R조상응적각시간점양성세포수( P <0.05)。【결론】대서뇌결혈재관주손상후단홍간예,기대서Hsp20적표체증가,뇌결혈후손상정도감경。
[Objective] To explore the expression of Hsp20 and the protective role of Danhong Injection in rat brain tissue after cerebral ischemic reperfusion .[Methods] A rat model of cerebral ischemia‐reperfusion was established through the method of middle cerebral artery occlusion .A total of 104 healthy male Sprague‐Dawley (SD) rats were randomly divided into normal control ,ischemia reperfusion (I/R) and Danhong injec‐tion intervention (D I/R) groups .And I/R and D I/R groups were sub‐divided into cerebral infarction and im‐mumohistochemistry groups .The expression of Hsp20 in brain tissue was detected by immunohistochemistry at 6 ,24 ,48 and 72h and Day 7 after IR in I/R and D I/R groups .All neurological deficit scores were assessed before sacrificing .And the experimental results were analyzed with Spss17 .0 .[Results] The cerebral infarct size was markedly larger in I/R group than that in D I/R group (105 .11 ± 10 .60 vs 82 .16 ± 7 .02 mm3 ) .And the difference was statistically significant ( P <0 .05) .The level of Hsp20 was evidently up‐regulated at 6h and peaked at 72h in I/R group ( P < 0 .05) .And the level of Hsp20 was evidently up‐regulated in D I/R group ( P<0 .05) .The neurological deficit scores of D I/R group were better than those of I/R group .[Con‐clusion] After ischemia‐reperfusion injury ,Danhong Injection may up‐regulate the level of Hsp20 and reduce the extent of ischemic damage .