Bacopa monnieri (L.) Ameliorates Cognitive Deficits Caused in a Trimethyltin-Induced Neurotoxicity Model Mice

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 pharmacologic...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2019/08/01, Vol.42(8), pp.1384-1393
Main Authors: Pham, Hang Thi Nguyet, Phan, Sinh Viet, Tran, Hong Nguyen, Phi, Xuyen Thi, Le, Xoan Thi, Nguyen, Khoi Minh, Fujiwara, Hironori, Yoneyama, Masanori, Ogita, Kiyokazu, Yamaguchi, Taro, Matsumoto, Kinzo
Format: Article
Language:English
Subjects:
Amygdala
Animal cognition
Animal memory
Animal models
Animals
anti-dementia effect
Bacopa
Bacopa monnieri (L.)
Brain slice preparation
Cognitive ability
Cognitive Dysfunction - drug therapy
Cognitive Dysfunction - pathology
Dementia
Dementia disorders
Dentate gyrus
Disease Models, Animal
Hippocampus
Hippocampus - drug effects
Hippocampus - pathology
Iodides
Male
Memory
Memory Disorders - drug therapy
Memory Disorders - pathology
Mice
Nerve Regeneration - drug effects
neurogenesis
Neurons
Neurons - drug effects
Neurons - pathology
Neuroprotective Agents - therapeutic use
Neurotoxicity
Neurotoxicity Syndromes - drug therapy
Neurotoxicity Syndromes - pathology
Plant Extracts - therapeutic use
Propidium iodide
Septum
Short term memory
Spatial memory
Staining
Synaptic plasticity
Trimethyltin
Trimethyltin Compounds
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Summary: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.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.b19-00288