海带多糖调节小鼠小胶质细胞活化保护放射损伤后的海马记忆功能

Laminaria japonica polysaccharides protects hippocampal memory after radiation by regulating microglia activation

目的:观察海带多糖(laminaria japonica polysaccharides,LJP)对小胶质细胞活性和放射诱导脑损伤后海马记忆功能的影响。方法:将120只2月龄雌性昆明小鼠随机分为对照组、LJP组、放射组、放射+LJP组,每组30只。用60Co射线制作小鼠的放射诱导脑损伤模型,LJP腹腔注射于放射前1 d进行,放射后4 d结束。采用Morris水迷宫观察LJP对放射后1 d、7 d、14 d小鼠空间记忆功能的影响;采用免疫组织化学法观察小胶质细胞标记物Iba-1的表达;ELISA检测海马中IL-1β、TNF-α含量。结果:放射后,小鼠在水迷宫中第1次找到平台的时间延长、穿越平台的次数减少(P<0.05);经LJP防治后的小鼠在各时间点找到平台的时间比放射组缩短、穿越平台的次数也增加(P<0.05);放射后1 d、7 d、14 d,放射组小鼠海马小胶质细胞胞体面积明显增大(P<0.01),细胞突起变粗、数量明显增多(P<0.01),IL-1β、TNF-α含量明显增多(P<0.05);经LJP处理后,与放射组相比,小胶质细胞突起逐渐变小,细胞面积和突起数量也减少,IL-1β、TNF-α含量减少(P<0.05)。LJP组和对照组未见差异。结论:LJP处理可以通过调节小胶质细胞活性、降低IL-1β、TNF-α含量保护放射损伤后的海马记忆功能。

Objective： To explore the effect of laminaria japonica polysaccharides（ LJP） on microglia and spatial memory of brain injury induced by radiation. Methods： 120 female Kunming mice（ 2-month-old） were randomly divided into 4 groups： control group,LJP group,radiation group and radiation ＋ LJP group. The model of radiation-induced brain injury of mice was established by60 Co γ ray. LJP intraperitoneal injection began at 1 d before radiation and until 4 d after radiation. The spatial memory of mice were assessed using Morris water mazes at 1 d,7 d and 14 d respectively following radiation. The expression of Iba-1 in hippocampus was observed with immunohistochemistry at the same time,respectively,together with IL-1β and TNF-α detected by ELISA. Results： The first time mice reaching to the platform was distinctly delayed（ P〈0. 05） at 1 d,7 d and 14 d following radiation,while times crossing the platform was visibly reduced（ P〈0. 05）. At the same time after radiation,the process of microglia became thicker,and the cell area and protuberance number of microglia was significantly increased（ P〈0. 01）,as well as the content of IL-1β and TNF-α（ P 〈0. 05）. However,after LJP treatment,the process of microglia became smaller,and the cell area and protuberance num-ber of microglia cells decreased compared with radiated mice,as well as the concentration of IL-1β and TNF-α decreased at the same time. No difference observed between control and LJP group. Conclusion： LJP may protect the hippocampal memory of radiation-induced brain injury by regulating microglial activity and decreasing the content of IL-1β and TNF-α.