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作 者:郭二坤[1] 梁朝辉[1] 彭立威[2] 刘志坤[3] 米中波 吕中强[1]
机构地区:[1]河北医科大学第二医院神经外科,石家庄050000 [2]河北医科大学第二医院神经内科,石家庄050000 [3]河北医科大学第四医院放疗科 [4]赵县人民医院神经外科
出 处:《脑与神经疾病杂志》2017年第12期757-760,共4页Journal of Brain and Nervous Diseases
摘 要:目的探讨姜黄素(Cur)对大鼠蛛网膜下腔出血(SAH)脑血管痉挛(CVS)的作用及其机制。方法将60只SD大鼠分成假手术组、SAH组及姜黄素+SAH组,每组20只,采用枕大池二次注血法制作SAH大鼠模型,姜黄素组在造模后给予一次姜黄素注射液(100mg·kg^(-1))腹腔注射治疗评定大鼠的神经生物功能,每组在造模后3d和7d处死,灌注固定后取大鼠基底动脉,印度墨水灌注,测量基底动脉内径、血管壁厚度,用酶联免疫吸附法测定各组血浆中肿瘤坏死因子-α(TNF-α)、一氧化氮酶(i NOS)含量。结果与假手术组相比,SAH组大鼠在造模后3d和7d基底动脉内径均显著缩小,基底动脉血管壁厚度显著增加,神经生物功能评分明显升高,血浆i NOS水平显著增高,TNF-α水平显著升高。与SAH组相比,使用姜黄素治疗后3d和7d基底动脉内径均显著增加,基底动脉血管壁厚度显著减小,神经生物功能评分降低,血浆i NOS水平显著降低,TNF-α水平显著降低。结论姜黄素可以改善SAH大鼠CVS,其机制可能与姜黄素抑制TNF-α和i NOS的信号通路,降低大鼠基底动脉血管炎症反应有关。Objective To investigate the effect of curcumin on cerebral vasospasm ( CVS ) in rats with subarachnoid hemorrhage ( SAH ) and possible mechanism. Method A total of 60 Sprague-Dawley rats were randomly divided into three groups ( Sham group, SAH group and eureumin one ) . Experimental SAH rat models were established by injecting autologous blood into the cisterna. Neurological deficits score of rats were examined at the third day and 7days after operation. Cognitive abilities were examined after operation. The diameter and inside diameter of basilal artery in rats models were measured after perfusion fixation at the day 3 and 7. Meanwhile, tumor necrosis factor-alpha ( TNF- α ) and inducible nitric oxide synthase ( iNOS ) were tested by ELISA. Results Cognitive abilities were significantly lower in experimental SAH rat models than in Sham group. The diameter and inside diameter of basal artery in rats models were thickened than Sham group, which indicated that the CVS seriously. The expression of TNF-α and iNOS were increased in the SAH group. In contrast to this, The diameter and inside diameter of basal artery in curcumin group were thinned than Sham group and SAH group, which indicated that the CVS alleviated. The expression of TNF-α and iNOS were decreased in the curcumin group. Conclusion Curcumin can relieved the CVS induced by SAH due to basilal artery inflammation through down-regulating TNF-α and iNOS levels.
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