现代医药卫生
現代醫藥衛生
현대의약위생
MODERN MEDICINE HEALTH
2014年
10期
1446-1448,1451
,共4页
脑缺血%再灌注损伤%川芎嗪%Toll样受体4%NF-κB%肿瘤坏死因子α%白细胞介素1β%大鼠, Sprague-Dawley
腦缺血%再灌註損傷%川芎嗪%Toll樣受體4%NF-κB%腫瘤壞死因子α%白細胞介素1β%大鼠, Sprague-Dawley
뇌결혈%재관주손상%천궁진%Toll양수체4%NF-κB%종류배사인자α%백세포개소1β%대서, Sprague-Dawley
Brain Ischemia%Reperfusion injury%Tetramethylpyrazine%Toll-like receptor 4%NF-kappa B%Tu-mor necrosis factor-alpha%Interleukin-1beta%Rats,sprague-dawley
目的：探讨川芎嗪对大鼠局灶性脑缺血再灌注损伤的保护作用及机制。方法将64只健康雄性SD大鼠随机分为四组：（1）假手术组；（2）缺血再灌注组；（3）川芎嗪20 mg/kg处理组；（4）川芎嗪40 mg/kg处理组。每组各16只，8只用于脑梗死体积测定，8只用于mRNA和蛋白的测定。采用线栓法制备大鼠局灶性大脑中动脉栓塞模型，缺血2 h再灌注24 h。术后对大鼠神经功能进行评分；2，3，5-氯化三苯四氮唑染色观察脑梗死体积；酶联免疫吸附法测定脑组织中肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）和核因子-κBp65（NF-κBp65）水平；实时定量聚合酶链反应和蛋白质印迹法分别检测Toll样受体4（TLR4） mRNA和蛋白的表达。结果与假手术组比较，缺血再灌注组大鼠的神经功能缺陷评分和脑梗死体积明显增加；脑组织中TNF-α、IL-1β和NF-κBp65水平以及TLR4的表达也显著升高，差异均有统计学意义（P<0.05）。川芎嗪处理组上述指标，与缺血再灌注组比较，差异有统计学意义（P<0.05）；不同剂量川芎嗪处理组间比较，差异无统计学意义（P>0.05）。结论川芎嗪可抑制脑缺血再灌注诱导的损伤，其机制与抑制TLR4/NF-κB信号通路，进而减少炎症因子的产生有关。
目的：探討川芎嗪對大鼠跼竈性腦缺血再灌註損傷的保護作用及機製。方法將64隻健康雄性SD大鼠隨機分為四組：（1）假手術組；（2）缺血再灌註組；（3）川芎嗪20 mg/kg處理組；（4）川芎嗪40 mg/kg處理組。每組各16隻，8隻用于腦梗死體積測定，8隻用于mRNA和蛋白的測定。採用線栓法製備大鼠跼竈性大腦中動脈栓塞模型，缺血2 h再灌註24 h。術後對大鼠神經功能進行評分；2，3，5-氯化三苯四氮唑染色觀察腦梗死體積；酶聯免疫吸附法測定腦組織中腫瘤壞死因子-α（TNF-α）、白介素-1β（IL-1β）和覈因子-κBp65（NF-κBp65）水平；實時定量聚閤酶鏈反應和蛋白質印跡法分彆檢測Toll樣受體4（TLR4） mRNA和蛋白的錶達。結果與假手術組比較，缺血再灌註組大鼠的神經功能缺陷評分和腦梗死體積明顯增加；腦組織中TNF-α、IL-1β和NF-κBp65水平以及TLR4的錶達也顯著升高，差異均有統計學意義（P<0.05）。川芎嗪處理組上述指標，與缺血再灌註組比較，差異有統計學意義（P<0.05）；不同劑量川芎嗪處理組間比較，差異無統計學意義（P>0.05）。結論川芎嗪可抑製腦缺血再灌註誘導的損傷，其機製與抑製TLR4/NF-κB信號通路，進而減少炎癥因子的產生有關。
목적：탐토천궁진대대서국조성뇌결혈재관주손상적보호작용급궤제。방법장64지건강웅성SD대서수궤분위사조：（1）가수술조；（2）결혈재관주조；（3）천궁진20 mg/kg처리조；（4）천궁진40 mg/kg처리조。매조각16지，8지용우뇌경사체적측정，8지용우mRNA화단백적측정。채용선전법제비대서국조성대뇌중동맥전새모형，결혈2 h재관주24 h。술후대대서신경공능진행평분；2，3，5-록화삼분사담서염색관찰뇌경사체적；매련면역흡부법측정뇌조직중종류배사인자-α（TNF-α）、백개소-1β（IL-1β）화핵인자-κBp65（NF-κBp65）수평；실시정량취합매련반응화단백질인적법분별검측Toll양수체4（TLR4） mRNA화단백적표체。결과여가수술조비교，결혈재관주조대서적신경공능결함평분화뇌경사체적명현증가；뇌조직중TNF-α、IL-1β화NF-κBp65수평이급TLR4적표체야현저승고，차이균유통계학의의（P<0.05）。천궁진처리조상술지표，여결혈재관주조비교，차이유통계학의의（P<0.05）；불동제량천궁진처리조간비교，차이무통계학의의（P>0.05）。결론천궁진가억제뇌결혈재관주유도적손상，기궤제여억제TLR4/NF-κB신호통로，진이감소염증인자적산생유관。
Objective To explore the protective effect and mechanism of ligustrazine on focal cerebral ischemia-reperfu-sion injury in rats. Methods Totally 64 healthy SD rats were divided into sham-operated group,ischemia-reperfusion group, 20 mg/kg ligustrazine group and 40 mg/kg ligustrazine group ,16 cases in each group including 8 cases for determination of volume of cerebral infarction and 8 cases for determination of mRNA and protein. Focal cerebral ischemia-reperfusion model in rats was made by suture-occluded method through 24 h reperfusion after 2 h of ischemia. The neurological function was scored after opera-tion and the infarct volume was measured by 2,3,5-Triphenyltetrazoliumchloride staining. The levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β) and nuclear factor-κBp65(NF-κBp65) in brain tissue were measured by enzyme linked im-munosorbent assay. The expression of Toll-likereceptor 4(TLR4) mRNA and protein was determined by real-time PCR and West-ern blotting,respectively. Results Compared with the sham-operated group,the neurological function score and infarct volume were significantly increased in ischemia-reperfusion group. The levels of TNF-α,IL-1βand NF-κBp65 in brain tissue and the ex-pression of TLR4 were also markedly increased with statistically significant difference (P<0.05). However,the above effects induced by ischemia-reperfusion were significantly inhibited by ligustrazine. The difference between 20 mg/kg ligustrazine group and 40 mg/kg ligustrazine group had no statistical significance(P>0.05),while the difference between ligustrazine groups and ischemia-reperfusion group was statistically significant(P<0.05). Conclusion Ligustrazine can inhibit cerebral ischemia-reperfusion injury, which might be related to decrease inflammatory factor production through inhibition of TLR4/NF-κB signal pathway.
