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Pharmaceutical Potential of Casein-Derived Tripeptide Met-Lys-Pro: Improvement in Cognitive Impairments and Suppression of Inflammation in APP/PS1 Mice
http://hdl.handle.net/10422/00013448
http://hdl.handle.net/10422/00013448e67a941e-4b54-4760-8f0d-eb88c6c26797
名前 / ファイル | ライセンス | アクション |
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2022-11-04 | |||||
タイトル | ||||||
タイトル | Pharmaceutical Potential of Casein-Derived Tripeptide Met-Lys-Pro: Improvement in Cognitive Impairments and Suppression of Inflammation in APP/PS1 Mice | |||||
言語 | en | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Alzheimer’s disease | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | APP/PS1 mice | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | dementia | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Met-Lys-Pro | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | MKP | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | peptide | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
アクセス権 | ||||||
アクセス権 | open access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||
著者 |
TADA-MATSUZAKI, Asuka
× TADA-MATSUZAKI, Asuka× HAMEZAH, Hamizah Shahirah Binti× ARROZI, Aslina PAHRUDIN× BAKAR, Zulzikry Hafiz Abu× YANAGISAWA, Daijiro× TOOYAMA, Ikuo |
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著者別名 |
多田, 明日翔
× 多田, 明日翔× 柳沢, 大治郎× 遠山, 育夫 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Background: Tripeptide Met-Lys-Pro (MKP), a component of casein hydrolysates, has effective angiotensin-converting enzyme (ACE) inhibitory activity. Brain angiotensin II enzyme activates the NADPH oxidase complex via angiotensin II receptor type 1 (AT1) and enhances oxidative stress injury. ACE inhibitors improved cognitive function in Alzheimer's disease (AD) mouse models and previous clinical trials. Thus, although undetermined, MKP may be effective against pathological amyloid-β (Aβ) accumulation-induced cognitive impairment. Objective: The current study aimed to investigate the potential of MKP as a pharmaceutical against AD by examining MKP's effect on cognitive function and molecular changes in the brain using double transgenic (APP/PS1) mice. Methods: Experimental procedures were conducted in APP/PS1 mice (n = 38) with a C57BL/6 background. A novel object recognition test was used to evaluate recognition memory. ELISA was used to measure insoluble Aβ40, Aβ42, and TNF-α levels in brain tissue. Immunohistochemical analysis allowed the assessment of glial cell activation in MKP-treated APP/PS1 mice. Results: The novel object recognition test revealed that MKP-treated APP/PS1 mice showed significant improvement in recognition memory. ELISA of brain tissue showed that MKP significantly reduced insoluble Aβ40, Aβ42, and TNF-α levels. Immunohistochemical analysis indicated the suppression of the marker for microglia and reactive astrocytes in MKP-treated APP/PS1 mice. Conclusion: Based on these results, we consider that MKP could ameliorate pathological Aβ accumulation-induced cognitive impairment in APP/PS1 mice. Furthermore, our findings suggest that MKP potentially contributes to preventing cognitive decline in AD. |
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言語 | en | |||||
書誌情報 |
en : Journal of Alzheimer's Disease 巻 89, 号 3, p. 835-848, 発行日 2022-09-27 |
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出版者 | ||||||
出版者 | IOS Press BV | |||||
言語 | en | |||||
ISSN | ||||||
収録物識別子タイプ | PISSN | |||||
収録物識別子 | 1387-2877 | |||||
PMID | ||||||
識別子タイプ | PMID | |||||
関連識別子 | 35964178 | |||||
PMCID | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | URI | |||||
関連識別子 | http://www.ncbi.nlm.nih.gov/pmc/articles/pmc9535549/ | |||||
言語 | en | |||||
関連名称 | PMC9535549 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.3233/jad-220192 | |||||
言語 | en | |||||
関連名称 | 10.3233/jad-220192 | |||||
権利 | ||||||
言語 | en | |||||
権利情報 | © 2022 – The authors. Published by IOS Press. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |