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胡黄连苷Ⅱ对大鼠脑缺血/再灌注损伤NF-κB和I-κB的干预作用 被引量:22

The interferring effects of picroside Ⅱ on the expressions of NF-κB and I-κB following cerebral ischemia reperfusion injury in rats
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摘要 目的研究胡黄连苷Ⅱ对大鼠脑缺血/再灌注后核转录因子κB(NF-κB)和NF-κB抑制因子(I-κB)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)和丹参素钠(10mg·kg-1)干预治疗,原位TUNEL检测神经细胞凋亡,免疫组化检测NF-κB和I-κB的表达,ELISA法检测脑组织匀浆NF-κB和I-κB的含量。结果假手术组大鼠皮质、纹状体和海马区脑组织NF-κB和I-κB弱表达,TUNEL阳性细胞数量较少,散在分布。阴性对照组大鼠各区脑组织TUNEL阳性细胞数量较假手术组均增多,NF-κB和I-κB表达增强,脑组织匀浆NF-κB和I-κB增高(P<0.05)。阳性对照组和胡黄连苷组各区脑组织TUNEL阳性细胞数量,NF-κB和I-κB表达(A值)及脑组织匀浆NF-κB和I-κB含量均低于阴性对照组(P<0.05),阳性对照组与胡黄连苷组比较,各指标差异均无显著性(P>0.05)。结论胡黄连苷Ⅱ可能通过下调NF-κB和I-κB的表达,抑制脑缺血/再灌注损伤的炎症反应导致的神经细胞凋亡。 Aim To study the interfering effects of picroside Ⅱ on the expressions of nuclear transcription factor kappaB(NF-κB)and inhibitor of NF-κB(I-κB) after cerebral ischemic reperfusion in rats. Methods Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion models in rats. PicrosideⅡ(10 mg·kg^-1) and salvianic acid A sodium(10 mg·kg^-1 ) were injected from the tail vein for treatment. TUNEL positive cells were counted by immunofluorescence assay. The expressions of NF-κB and I-κB were determined by immunohistochemical assay,and the concentration of NF-κB and I-κB in brain tissue was determined by ELISA. Results The exprssions of NF-κB and I-κB were weakly and the apoptotic cells were scattering at cortex,striatum and hip-pocampus in the sham operative group. In the negative control group,the number of TUNEL positive cells and the expressions of NF-κB and I-κB increased,the absorption(A) values and the concentration were significantly higher than those in the sham operative group(P〈0.05). While in the positive control and picroside groups,the expressions(A values)and concentration of NF-κB and I-κB and the number of TUNEL positive cells were significantly lower than those in the negative control group (P〈0.05 ). There was no significant difference between the positive control group and picro-side group ( P〉0.05 ). Conclusion Picroside Ⅱ might downregulate the expressions of NF-κB and I-κB to inhibit neuronal apoptosis induced by inflammation after cerebral ischemia reperfusion injury in rats.
出处 《中国药理学通报》 CAS CSCD 北大核心 2010年第1期52-56,共5页 Chinese Pharmacological Bulletin
基金 国家自然科学基金资助项目(No30873391)
关键词 胡黄连苷Ⅱ 脑缺血 再灌注损伤 核转录因子-ΚB NF-κB抑制因子 细胞凋亡 ELISA 大鼠 picrosideⅡ cerebral ischemia reperfusion injury NF-κB I-κB apoptosis ELISA rats
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