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作 者:任冬青[1] 丁培炎[1] 岳海源[2] 陈岩松[2] 李亚萍[1] 唐慧如[2] 阎文军[1]
机构地区:[1]甘肃省人民医院麻醉科,兰州市730030 [2]兰州大学第二医院
出 处:《临床麻醉学杂志》2015年第4期379-382,共4页Journal of Clinical Anesthesiology
基 金:国家自然科学基金(81360193)
摘 要:目的探讨黄芪多糖对肝叶部分切除小鼠术后认知功能及p38MAPK磷酸化的影响。方法老年雄性昆明小鼠随机分为假手术组(S组)、手术组(O组)和黄芪多糖+手术组(A组)。术后1、3、7d,采用Morris水迷宫检测小鼠学习认知功能;采用Western blot技术检测小鼠海马区p38MAPK磷酸化水平。结果术后3d和7d,与S组比较,O组潜伏期明显延长(P<0.01),穿台次数明显减少(P<0.01或P<0.05),在目标象限停留时间明显缩短(P<0.01);与O组比较,A组潜伏期明显缩短,穿台次数明显增加,在目标象限停留时间明显延长(P<0.05)。术后1、3、7d,O组p38MAPK磷酸化水平明显升高(P<0.05);与O组比较,A组p38MAPK磷酸化水平明显下降(P<0.05或P<0.01)。术后1、3、7d各组p38MAPK蛋白表达总水平差异无统计学意义。结论黄芪多糖能够明显改善肝叶部分切除小鼠术后认知功能障碍,其机制可能与其抑制p38MAPK蛋白异常磷酸化有关。Objective To evaluate the effects of astragalus polysaccharides (APS) on cognitive function and p38MAPK phosphorylation in mice after partial hepatectomy. Methods The Kunming eldly male mice were randomly assigned to three groups: sham operation group (group S), operation group (group O) and APS treatment group (group A). The cognitive function was detected by Morris water maze test; the expression of p38MAPK phosphorylation in hippocampus was measured by Western blot on day 1, day 2 and day 7 after partial hepatectomy respectively. Results Compared with group S, the escape latency was significantly increased (P〈0.01), time spent in target quadrant and the number of platform-site crossovers were significantly decreased in group O on 3 d and 7 d after partial hepatectomy (P〈0. 01 or P〈0. 05); compared with group O, the escape latency was signifi- cantly decreased (P〈0.05), time spent in target quadrant and the number of platform-site crossovers were significantly increased in group A (P〈0. 05). Western blot showed that the phosphorylation of p38MAPK in group O was obviously increased on 1 d, 3 d and 7 d after partial hepatectomy, compared with group O, the phosphorylation of p38MAPK in group A was significantly decreased (P〈0.05 or P〈0. 01), and the expression of total p38MAPK was not significantly changed on 1 d, 3 d and 7 d after partial hepatectomy. Conclusion APS can significantly improve postoperative cognitive dysfunction in mice after partial hepateetomy, and the mechanism may be related to the inhibition of p38MAPK hyper-phosphorylation.
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