Dun Changping, Liu Junqian, Qiu Fucheng, Wu Xueda, Wang Yakun, Zhao Yongyan, Gu Ping
Department of Neurology, the First Hospital of Hebei Medical University.
Department of Cardiac Surgery, the Second Hospital of Hebei Medical University.
Neuropsychiatr Dis Treat. 2016 Jul 1;12:1617-21. doi: 10.2147/NDT.S106123. eCollection 2016.
Astragalus polysaccharides (APS) are active constituents of Astragalus membranaceus. In this study, we aimed to investigate the effects of APS on memory impairment in a diabetic rat model and their mechanisms.
A diabetic model was established in 50 male Wistar rats with streptozotocin intra-peritoneal injection. A blood glucose level higher than 16.7 mmol/L obtained 72 hours after the injection was regarded as a successful diabetic model. The modeled rats were divided into model group, high, medium, and low doses of APS, and piracetam groups (positive control). A group of ten rats without streptozotocin-induced diabetes were used as a normal control. After respective consecutive 8-week treatments, the levels of blood fasting plasma glucose, insulin, hemoglobin A1c, memory performance, hippocampal malondialdehyde, and superoxide dismutase were determined.
After the 8-week APS treatment, serum fasting plasma glucose, hemoglobin A1c, and insulin levels were decreased compared with those of the model group (P<0.05). Importantly, memory impairment in the diabetic model was reversed by APS treatments. In addition, hippocampal malondialdehyde concentration was lowered, whereas that of superoxide dismutase was higher after APS treatments.
APS are important active components responsible for memory improvement in rats with streptozotocin-induced diabetes. The potential mechanism of action is associated with the effects of APS on glucose and lipid metabolism, and antioxidative and insulin resistance. APS are constituents of A. membranaceus that are potential candidate therapeutic agents for the treatment of memory deficit in diabetes.
黄芪多糖（APS）是黄芪的活性成分。在本研究中，我们旨在探讨APS对糖尿病大鼠模型记忆损伤的影响及其机制。
采用腹腔注射链脲佐菌素的方法，在50只雄性Wistar大鼠中建立糖尿病模型。注射后72小时测得血糖水平高于16.7 mmol/L被视为糖尿病模型成功建立。将造模成功的大鼠分为模型组、高、中、低剂量APS组以及吡拉西坦组（阳性对照）。选取10只未注射链脲佐菌素诱导糖尿病的大鼠作为正常对照组。连续8周进行相应处理后，测定空腹血糖、胰岛素、糖化血红蛋白、记忆能力、海马丙二醛和超氧化物歧化酶水平。
经过8周的APS治疗，与模型组相比，血清空腹血糖、糖化血红蛋白和胰岛素水平均有所降低（P<0.05）。重要的是，APS治疗可逆转糖尿病模型中的记忆损伤。此外，APS治疗后海马丙二醛浓度降低，而超氧化物歧化酶浓度升高。
APS是链脲佐菌素诱导糖尿病大鼠记忆改善的重要活性成分。其潜在作用机制与APS对糖脂代谢、抗氧化及胰岛素抵抗的影响有关。APS是黄芪的成分，是治疗糖尿病记忆缺陷的潜在候选治疗药物。
