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机构地区:[1]北京中医药大学第一临床医学院中西医结合临床教研室,北京100029 [2]中国医学科学院北京协和医院中医科,北京100730
出 处:《中国医科大学学报》2009年第9期677-680,共4页Journal of China Medical University
基 金:卫生部中医药管理局中国中医药科学技术专项基金资助项目(0405LL01)
摘 要:目的探讨糖尿病认知功能障碍的发病机制及寻找有效的治疗用药。方法采用链脲佐菌素(STZ)诱发糖尿病大鼠模型。将大鼠随机分为正常组、模型组、中药脑复聪高、中、低剂量治疗组。通过水迷宫实验观察大鼠学习记忆能力,并于8周后取脑组织行胰岛素样生长因子Ⅰ(IGF-Ⅰ)免疫组织化学染色。结果模型组水迷宫的潜伏期较正常组延长(P<0.01),海马CA1区内IGF-Ⅰ阳性细胞数目减少(P<0.01);脑复聪治疗组大鼠的水迷宫潜伏期均短于模型组(P<0.01),且与脑复聪剂量呈负相关(P<0.01),治疗组大鼠海马CA1区内IGF-Ⅰ阳性细胞数目均增多(P<0.01),且与脑复聪剂量呈正相关(P<0.01)。结论糖尿病大鼠存在学习记忆能力的下降及海马CA1区IGF-Ⅰ含量的减少,而海马CA1区IGF-Ⅰ含量的减少可能是糖尿病大鼠学习记忆能力的下降的机制之一;脑复聪可改善糖尿病大鼠学习记忆能力,其机制可能与增加海马CA1区IGF-Ⅰ的含量有关。Objective To study the mechanism of diabetes-related cognitive impairment and search for effective clinical treatment with traditional Chinese medicine. Methods Diabetes model rats were induced by streptozotocin (STZ),and treated with high,middle and low dosage Naofucong grains. Abilities of learning and memory were tested with Morris water maze. Numbers of insulin-like growth factor-Ⅰ(IGF-Ⅰ )positive cells in hippocampus CA1 region were detected with immunohistochemical method. Results The incubation periods of diabetes model rats were longer than those of the normal mts(P 〈 0.01 ). The number of IGF-Ⅰ positive cells in hippocampus CA1 region of diabetes model rats was less than that of the normal rats(P 〈 0.01 ). The incubation periods of diabetes rats treated with Naofucong grain administration were shorter than those of diabetes model rats without Naofucong treatment(P 〈 0.01 ). Numbers of IGF- Ⅰ positive cells in hippocampus CA1 region of rats treated with Naofucong were more than that of diabetes model rats without Naofucong treatment (P 〈 0.01 ). Conclusion The diabetes model rat's abilities of learning and memory have been weakened, and the contents of IGF- Ⅰ in hippocampus CA1 region were deduced. It may be one of the mechanisms of the impairment of leanfing and memory abilities in diabetes model rats. Naofucong grains can improve diabetes rat' s abilities of learning and memory, and its mechanism may be related to the augment of the content of IGF- Ⅰ.
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