王展,郭峰君,史姣霞,等.海带岩藻聚糖硫酸酯对栓塞性脑缺血损伤的保护及作用机制的研究D[J].中国海洋药物,2018,37(1):55-61.
海带岩藻聚糖硫酸酯对栓塞性脑缺血损伤的保护及作用机制的研究D
Protective activity of fucoidan from Laminaria japonica on the thromboembolic cerebral ischemia injury and its possible mechanism
投稿时间:2017-07-26  修订日期:2017-12-01
DOI:
中文关键词:  岩藻聚糖硫酸酯  低分子量岩藻聚糖硫酸酯  栓塞性脑缺血损伤
English Keywords:fucoidan  low molecular weight fucoidan  thromboembolic cerebral ischemia injury
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作者单位E-mail
王展 青岛市中心医院 940361395@ouc.edu.cn 
郭峰君 食品科学与工程学院  
史姣霞 食品科学与工程学院  
于彤 食品科学与工程学院  
赵雪 食品科学与工程学院  
孙锋* 青岛市中心医院 sunfengsong@163.com 
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中文摘要:
      目的 对不同分子量海带岩藻聚糖硫酸酯对大鼠栓塞性脑缺血损伤的保护活性及其作用机制进行研究比较。方法 以海带高分子量和低分子量岩藻聚糖硫酸酯为研究对象,采用电刺激造栓法建立大鼠动脉栓塞性脑缺血损伤模型,观察岩藻聚糖硫酸酯对神经行为学评分、脑梗死体积、大脑皮层形态学、血液中花生四烯酸代谢产物(TXB2和6-kelo-PGF1α)、磷脂代谢产物(PA和LPA)和纤溶系统(t-PA和u-PA)的影响。结果 静脉注射高分子量和低分子量岩藻聚糖硫酸酯对大鼠栓塞性脑缺血损伤具有很好的保护作用,显著降低神经行为学评分、脑梗死体积和脑皮层神经细胞的损伤,低分子量岩藻聚糖硫酸酯的保护活性是高分子量组分的1/10。岩藻聚糖硫酸酯预防栓塞性脑缺血损伤的作用机理为:抑制TXB2生成,提高6-kelo-PGF1α的水平,抑制LPA的释放,从而抑制血栓的进一步发展;促进t-PA和u-PA的生成从而激活纤溶系统。结论:岩藻聚糖硫酸酯在预防栓塞性脑缺血损伤方面具有很好的应用潜质。
English Summary:
      Objective To study the protective activity of the high molecular weight (HMW) fucoidan and low molecular weight (LMW) fucoidan from Laminaria japonica on thromboembolic cerebral ischemia injury and possible action mechanism. Methods With the HMW fucoidan and LMW fucoidan from Laminaria japonica as the research objective, the thromboembolic cerebral ischemia injury model was induced by the electricity-stimulated carotid thrombosis in rats, and intravenous administration method was adopted. After inject, the neurological grade evaluation, volumn of cerebral infraction, morphology of brain cortex and the content of TXB2, 6-keto-PGF1α, t-PA, u-PA, PA and LPA in the blood were measured. Results HMW fucoidan and LMW fucoidan from Laminaria japonica were effective in preventing the thromboembolic cerebral ischemia injury. Intravenous administration of HMW fucoidan and LMW fucoidan significantly decreased the scores of neurological grade, volumn of cerebral infraction and the damage of cerebral cortex neurons, accompanied with alleviates of cerebral edema injury induced by thromboembolic cerebral ischemia in rats. Our result showed that the protective activity of LMW fucoidan was only 10% of HMW fucoidan. Under the effective protection concentration, the protective mechanism on the thromboembolic cerebral ischemia injury of HMW fucoidan and LMW fucoidan might be ascribe to the inhibition of TXB2 and LPA levels and promotion of 6-keto-PGF1α, t-PA and u-PA levels. Conclusion Fucoidan and LMW fucoidan had excellent protective activity on the thromboembolic cerebral ischemia injury in vivo.
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