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

• Pham Hang Thi Nguyet

  National Institute of Medicinal Materials

• Phan Sinh Viet

  National Geriatric Hospital

• Tran Hong Nguyen

  National Institute of Medicinal Materials

• Phi Xuyen Thi

  National Institute of Medicinal Materials

• Le Xoan Thi

  National Institute of Medicinal Materials

• Nguyen Khoi Minh

  National Institute of Medicinal Materials

• Fujiwara Hironori

  Division of Medicinal Pharmacology, Institute of Natural Medicine, University of Toyama

• Yoneyama Masanori

  Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University

• Ogita Kiyokazu

  Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University

• Yamaguchi Taro

  Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University

• Matsumoto Kinzo

  Division of Medicinal Pharmacology, Institute of Natural Medicine, University of Toyama

書誌事項

タイトル別名

• <i>Bacopa monnieri</i> (L.) Ameliorates Cognitive Deficits Caused in a Trimethyltin-Induced Neurotoxicity Model Mice

抄録

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.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 42 (8), 1384-1393, 2019-08-01

  公益社団法人 日本薬学会

キーワード

• <i>Bacopa monnieri</i> (L.)
• anti-dementia effect
• trimethyltin
• neurogenesis
• hippocampus
• dentate gyrus

詳細情報

• CRID: 1390845713086024064
• NII論文ID: 130007686678
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.b19-00288
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 029840763
• PubMed: 31366873
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I029840763
• Web Site: https://www.jstage.jst.go.jp/article/bpb/42/8/42_b19-00288/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2020123155
• 本文言語コード: en
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
  • KAKEN
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