Cui S Q, Wang Q, Zheng Y, Xiao B, Sun H W, Gu X L, Zhang Y C, Fu C H, Dong P X, Wang X M
China Shandong Provincial Engineering Laboratory of New Pharmaceutical Excipients, Sustained and Controlled Release Technology, College of Medicine and Nursing, Dezhou University, Dezhou, China.
Department of Physiology, Capital Medical University, Beijing, China.
Braz J Med Biol Res. 2015 Jun;48(6):515-22. doi: 10.1590/1414-431X20144250. Epub 2015 Mar 27.
We evaluated the effect of puerarin on spatial learning and memory ability of mice with chronic alcohol poisoning. A total of 30 male C57BL/6 mice were randomly divided into model, puerarin, and control groups (n=10 each). The model group received 60% (v/v) ethanol by intragastric administration followed by intraperitoneal injection of normal saline 30 min later. The puerarin group received intragastric 60% ethanol followed by intraperitoneal puerarin 30 min later, and the control group received intragastric saline followed by intraperitoneal saline. Six weeks after treatment, the Morris water maze and Tru Scan behavioral tests and immunofluorescence staining of cerebral cortex and hippocampal neurons (by Neu-N) and microglia (by Ib1) were conducted. Glutamic acid (Glu) and gamma amino butyric acid (GABA) in the cortex and hippocampus were assayed by high-performance liquid chromatography (HPLC), and tumor necrosis factor (TNF)-α and interleukin (IL)-1β were determined by ELISA. Compared with mice in the control group, escape latency and distance were prolonged, and spontaneous movement distance was shortened (P<0.05) by puerarin. The number of microglia was increased in both the cortex and hippocampal dentate gyrus (P<0.01), and neurons were reduced only in the hippocampal dentate gyrus (P<0.01) in puerarin-treated mice. In the model group, Glu and GABA levels decreased (P<0.05), and Glu/GABA, TNF-α, and IL-1β increased (P<0.01) with puerarin treatment, returning to near normal levels. In conclusion, puerarin protected against the effects of chronic alcohol poisoning on spatial learning and memory ability primarily because of anti-inflammatory activity and regulation of the balance of Glu and GABA.
我们评估了葛根素对慢性酒精中毒小鼠空间学习和记忆能力的影响。将30只雄性C57BL/6小鼠随机分为模型组、葛根素组和对照组（每组n = 10）。模型组通过灌胃给予60%（v/v）乙醇，30分钟后腹腔注射生理盐水。葛根素组灌胃60%乙醇，30分钟后腹腔注射葛根素，对照组灌胃生理盐水，随后腹腔注射生理盐水。治疗6周后，进行莫里斯水迷宫和Tru Scan行为测试，并对大脑皮层和海马神经元（通过Neu-N）以及小胶质细胞（通过Ib1）进行免疫荧光染色。采用高效液相色谱法（HPLC）测定皮层和海马中的谷氨酸（Glu）和γ-氨基丁酸（GABA），并通过酶联免疫吸附测定法（ELISA）测定肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1β。与对照组小鼠相比，葛根素使逃避潜伏期和距离延长，自发运动距离缩短（P<0.05）。葛根素处理的小鼠皮层和海马齿状回中的小胶质细胞数量增加（P<0.01），仅海马齿状回中的神经元数量减少（P<0.01）。在模型组中，葛根素治疗后Glu和GABA水平降低（P<0.05），Glu/GABA、TNF-α和IL-1β升高（P<0.01），恢复至接近正常水平。总之，葛根素可预防慢性酒精中毒对空间学习和记忆能力的影响，主要是由于其抗炎活性以及对Glu和GABA平衡的调节作用。
