Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Chotosan (Diaoteng San)-induced improvement of cognitive deficits in senescence-accelerated mouse (SAMP8) involves the amelioration of angiogenic/neurotrophic factors and neuroplasticity systems in the brain. | Zhao et al. Chinese Medicine 2011 6 33 http content 6 1 33 CHINESE MEDICINE RESEARCH Open Access Chotosan Diaoteng San -induced improvement of cognitive deficits in senescence-accelerated mouse SAMP8 involves the amelioration of angiogenic neurotrophic factors and neuroplasticity systems in the brain Qi Zhao1 2 Takako Yokozawa2 3 Koichi Tsuneyama4 Ken Tanaka5 Takeshi Miyata6 7 Notoshi Shibahara2 and Kinzo Matsumoto 1 Abstract Background Chotosan CTS Diaoteng San a Kampo medicine ie Chinese medicine formula is reportedly effective in the treatment of patients with cerebral ischemic insults. This study aims to evaluate the therapeutic potential of CTS in cognitive deficits and investigates the effects and molecular mechanism s of CTS on learning and memory deficits and emotional abnormality in an animal aging model namely 20-week-old senescence-accelerated prone mice SAMP8 with and without a transient ischemic insult T2VO . Methods Age-matched senescence-resistant inbred strain mice SAMR1 were used as control. SAMP8 received T2VO T2VO-SAMP8 or sham operation sham-SAMP8 at day 0. These SAMP8 groups were administered CTS 750 mg kg . or water daily for three weeks from day 3. Results Compared with the control group both sham-SAMP8 and T2VO-SAMP8 groups exhibited cognitive deficits in the object discrimination and water maze tests and emotional abnormality in the elevated plus maze test. T2VO significantly exacerbated spatial cognitive deficits of SAMP8 elucidated by the water maze test. CTS administration ameliorated the cognitive deficits and emotional abnormality of sham- and T2VO-SAMP8 groups. Western blotting and immunohistochemical studies revealed a marked decrease in the levels of phosphorylated forms of neuroplasticity-related proteins N-methyl-D-aspartate receptor 1 NMDAR1 Ca2 calmodulin-dependent protein kinase II CaMKII cyclic AMP responsive element binding protein CREB and brain-derived neurotrophic factor BDNF in the frontal cortices of
