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Total saponins from Rhizoma Anemarrhenae ameliorate diabetes-associated cognitive decline in rats: Involvement of amyloid-beta decrease in brain

Liu, Yao-Wu, Zhu, Xia, Lu, Qian, Wang, Jian-Yun, Li, Wei, Wei, Ya-Qin, Yin, Xiao-Xing
Journal of ethnopharmacology 2012 v.139 no.1 pp. 194-200
blood, blood glucose, body weight, cognition, cortex, diabetes, encephalitis, hippocampus, homeopathic drugs, intraperitoneal injection, rats, saponins, tumor necrosis factor-alpha
ETHNOPHARMACOLOGICAL RELEVANCE: As a well-known Chinese Materia Medica Rhizoma Anemarrhenae has multiple pharmacological activities including antipyretic, anti-inflammatory, anti-diabetic actions, etc. This study was designed to investigate effects of total saponins from Rhizoma Anemarrhenae (TS) on diabetes-associated cognitive decline in rats and influence on amyloid-beta (Aβ) levels in brain and inflammation. MATERIALS AND METHODS: Diabetic rats induced by intraperitoneal administration of streptozotocin, were randomized into two groups: diabetes and TS-treated diabetes. Blood glucose and body weight were measured monthly and weekly, respectively. After seven weeks, cognitive performances were evaluated with Morris water maze. Then, brain was obtained for assay of Aβ and TNF-α levels, and blood was collected for TNF-α assay. RESULTS: Aβ(1–40), Aβ(1–42) and TNF-α levels were dramatically (all P<0.01) increased both in temporal cortex and hippocampus of diabetic rats, coupled with impairment of cognition, compared with those of the control. Chronic TS (200mg/kg) treatment markedly (P<0.05) improved the learning ability of diabetic rats, and significantly (all P<0.05) reduced Aβ(1–40), Aβ(1–42) and TNF-α levels in cortex as well as Aβ(1–40) level in hippocampus, whereas showed a decreased tendency for Aβ(1–42) and TNF-α levels in hippocampus. Moreover, eight-week treatment with TS remarkably (P<0.05) inhibited the elevation of TNF-α level in serum of diabetic rats, and significantly (both P<0.01) decrease the fasting blood glucose level and increase the body weight of diabectic rats. CONCLUSION: Our findings demonstrate that diabetes-associated cognitive decline is, at least in part, due to brain Aβ accumulation in diabetic condition, and efficacy of TS to diabetes-associated cognitive decline in rats is a sum of reduction of Aβ accumulation and inflammation in brain as well as attenuation of major symptoms of diabetes.