Bacopa monnieri (L.) Ameliorates Cognitive Deficits Caused in a Trimethyltin-Induced Neurotoxicity Model Mice
Autor: | Taro Yamaguchi, Hang Thi Nguyet Pham, Khoi Minh Nguyen, Xuyen Thi Phi, Hong Nguyen Tran, Kinzo Matsumoto, Xoan Thi Le, Kiyokazu Ogita, Sinh Viet Phan, Hironori Fujiwara, Masanori Yoneyama |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Pharmacology biology business.industry Dentate gyrus Neurogenesis Neurotoxicity Pharmaceutical Science Hippocampus General Medicine Hippocampal formation medicine.disease biology.organism_classification Neuroregeneration 03 medical and health sciences 030104 developmental biology 0302 clinical medicine 030220 oncology & carcinogenesis medicine Bacopa monnieri Cholinergic neuron business |
Zdroj: | Biological and Pharmaceutical Bulletin. 42:1384-1393 |
ISSN: | 1347-5215 0918-6158 |
Popis: | We previously demonstrated that Bacopa monnier (L.) WETTST. extract (BME) ameliorated cognitive dysfunction in animal models of dementia by enhancing synaptic plasticity-related signaling in the hippocampus and protecting cholinergic neurons in the medial septum. To further clarify the pharmacological features and availability of BME as a novel anti-dementia agent, we investigated whether BME affects neuronal repair using a mouse model of trimethyltin (TMT)-induced neuronal loss/self-repair in the hippocampus. Mice pretreated with TMT (2.8 mg/kg, intraperitoneally (i.p.)) on day 0 were given BME (50 mg/kg, per os (p.o.)) once daily for 15-30 d. Cognitive performance of the animals was elucidated twice by the object location test and modified Y maze test on days 17-20 (Phase I) and days 32-35 (Phase II) or by the passive avoidance test on Phase II. TMT impaired hippocampus-dependent spatial working memory and amygdala-dependent fear-motivated memory. The administration of BME significantly prevented TMT-induced cognitive deficits. The protective effects of BME on the spatial memory deficits were confirmed by Nissl staining of hippocampal tissues and propidium iodide staining of organotypic hippocampal slice cultures. Immunohistochemical studies conducted on days 17 and 32 revealed that thirty days of treatment with BME increased the number of 5-bromo-2'-deoxyuridine (BrdU)-immunopositive cells in the dentate gyrus region of TMT-treated mice, whereas fifteen days of treatment with BME had no effect. These results suggest that BME ameliorates TMT-induced cognition dysfunction mainly via protecting the hippocampal neurons from TMT-induced hippocampal lesions and partly via promoting neuroregeneration in the dentate gyrus regions. |
Databáze: | OpenAIRE |
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