摘要
目的:研究黄连苷Ⅱ对大鼠脑缺血后细胞凋亡和NFκB表达的影响。方法:应用线栓法建立大鼠大脑中动脉闭塞再灌注模型,经尾静脉注射胡黄连苷Ⅱ(10mg.kg-1)干预治疗,免疫组化检测脑缺血再灌注后核转录因子κB(NFκB)表达,原位缺口末端标记(TUNEL)检测神经细胞凋亡。结果:假手术组大鼠皮质、纹状体和海马区脑组织NFκB,TUNEL阳性细胞数量较少,散在分布。模型组大鼠各区脑组织NFκB表达显著增强,吸光度值(A)和TUNEL阳性细胞数量较假手术组均显著增多(P<0.05)。胡黄连苷组各区脑组织NFκB(A值)及TUNEL阳性细胞数量均显著低于模型对照组(P<0.05)。结论:胡黄连苷Ⅱ可能通过下调NFκB的表达,抑制脑缺血再灌注损伤炎症反应导致的神经细胞凋亡。
OBJECTIVE To sludy the effect of picroside Ⅱ on the apoptosis and expressions of nuclear transcription factor kappaB （NFκB） after cerebral ischemia in rats. METHODS The middle cerebral artery occlusion reperfusion models in rats were established by intraluminal thread methods and treated by injecting Picroside-Ⅱ （10mg·kg-1 ） from the tail vein. The expression of NFκB was determined by immunohistochemical assay and the apoptotic positive cells were counted by terminal deoxynucleotidyl transference mediated biotinylated deoxyuridine triphosphate nick end labeling technique （TUNEL）. RESULTS The results shown that exprssions of NFκB were weakly and the apoptotic cells were scattering at cortex, striatum and hippocampus in the sham operative group. In the model control group, the expressions of NFκB increased, the absorption （A） values and the number of TUNEI. positive cells were significantly higher than those in the sham operative group （P〈0. 05）. While in pieroside groups, the expressions （A values） of NFκB and the number of TUNEL positive cells were significantly lower than those in the model control group （P〈0. 05）. CONCLUSION The results suggested that picroside Ⅱ might down regulate the expressions of NFκB to inhibit neuronal apoptosis induced by inflammation after cerebral ischomia reperfusion injury in rats.
出处
《中国医院药学杂志》
CAS
CSCD
北大核心
2010年第17期1457-1459,共3页
Chinese Journal of Hospital Pharmacy
