Neurotrophic Effect of Magnolol in the Hippocampal CA1 Region of Senescence-Accelerated Mice (SAMP1)
Magnolol has neurotrophic effects in primary cultured rat cortical neurons, which are expressed as the promotion of neurite outgrowth and neuronal survival. In this study, we investigated the protective effect of magnolol against age-related neuronal loss in the hippocampus using senescence-accelera...
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Veröffentlicht in: | Biological & Pharmaceutical Bulletin 2005, Vol.28(9), pp.1762-1765 |
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creator | Matsui, Nobuaki Nakashima, Hiroshi Ushio, Yuki Tada, Toshimasa Shirono, Akiko Fukuyama, Yoshiyasu Nakade, Kousuke Zhai, Haifeng Yasui, Yumiko Fukuishi, Nobuyuki Akagi, Reiko Akagi, Masaaki |
description | Magnolol has neurotrophic effects in primary cultured rat cortical neurons, which are expressed as the promotion of neurite outgrowth and neuronal survival. In this study, we investigated the protective effect of magnolol against age-related neuronal loss in the hippocampus using senescence-accelerated mouse (SAMP1). Magnolol (5, 10 mg/kg) was orally administered once a day for 14 d to 2- or 4-month-old mice, and evaluation was carried out when the mice were 4 or 6 months old. The density of neurofibrils decreased with aging in the stratum radiatum of the CA1 region in the hippocampus of SAMP1, not SAMR1. Treatment with magnolol significantly prevented the decrease of neurofibrils in the CA1, when it was administered in 2-month-olds. However, administration at 4 months of age did not result in a preventive effect. These findings suggest that the administration of magnolol before the initiation of neuronal loss may result in a protective effect in the hippocampus. |
doi_str_mv | 10.1248/bpb.28.1762 |
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In this study, we investigated the protective effect of magnolol against age-related neuronal loss in the hippocampus using senescence-accelerated mouse (SAMP1). Magnolol (5, 10 mg/kg) was orally administered once a day for 14 d to 2- or 4-month-old mice, and evaluation was carried out when the mice were 4 or 6 months old. The density of neurofibrils decreased with aging in the stratum radiatum of the CA1 region in the hippocampus of SAMP1, not SAMR1. Treatment with magnolol significantly prevented the decrease of neurofibrils in the CA1, when it was administered in 2-month-olds. However, administration at 4 months of age did not result in a preventive effect. These findings suggest that the administration of magnolol before the initiation of neuronal loss may result in a protective effect in the hippocampus.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.28.1762</identifier><identifier>PMID: 16141555</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>Aging - drug effects ; Aging - genetics ; Aging - pathology ; Animals ; Biphenyl Compounds - pharmacology ; Cell Count ; hippocampus ; Hippocampus - cytology ; Hippocampus - drug effects ; Hippocampus - pathology ; Lignans - pharmacology ; magnolol ; Mice ; Mice, Inbred Strains ; Nerve Degeneration - pathology ; Neurites - drug effects ; Neurofibrils - drug effects ; senescence accelerated mouse ; Tissue Embedding</subject><ispartof>Biological and Pharmaceutical Bulletin, 2005, Vol.28(9), pp.1762-1765</ispartof><rights>2005 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c720t-fe35df80ebddd6f7dcfdd8daebee9156ab135e5845875f12c51bc43509ae6d4a3</citedby><cites>FETCH-LOGICAL-c720t-fe35df80ebddd6f7dcfdd8daebee9156ab135e5845875f12c51bc43509ae6d4a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16141555$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsui, Nobuaki</creatorcontrib><creatorcontrib>Nakashima, Hiroshi</creatorcontrib><creatorcontrib>Ushio, Yuki</creatorcontrib><creatorcontrib>Tada, Toshimasa</creatorcontrib><creatorcontrib>Shirono, Akiko</creatorcontrib><creatorcontrib>Fukuyama, Yoshiyasu</creatorcontrib><creatorcontrib>Nakade, Kousuke</creatorcontrib><creatorcontrib>Zhai, Haifeng</creatorcontrib><creatorcontrib>Yasui, Yumiko</creatorcontrib><creatorcontrib>Fukuishi, Nobuyuki</creatorcontrib><creatorcontrib>Akagi, Reiko</creatorcontrib><creatorcontrib>Akagi, Masaaki</creatorcontrib><creatorcontrib>Tokushima Bunri University</creatorcontrib><creatorcontrib>bFaculty of Health and Welfare Science</creatorcontrib><creatorcontrib>Okayama Prefectural University</creatorcontrib><creatorcontrib>aFaculty of Pharmaceutical Sciences</creatorcontrib><title>Neurotrophic Effect of Magnolol in the Hippocampal CA1 Region of Senescence-Accelerated Mice (SAMP1)</title><title>Biological & Pharmaceutical Bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>Magnolol has neurotrophic effects in primary cultured rat cortical neurons, which are expressed as the promotion of neurite outgrowth and neuronal survival. In this study, we investigated the protective effect of magnolol against age-related neuronal loss in the hippocampus using senescence-accelerated mouse (SAMP1). Magnolol (5, 10 mg/kg) was orally administered once a day for 14 d to 2- or 4-month-old mice, and evaluation was carried out when the mice were 4 or 6 months old. The density of neurofibrils decreased with aging in the stratum radiatum of the CA1 region in the hippocampus of SAMP1, not SAMR1. Treatment with magnolol significantly prevented the decrease of neurofibrils in the CA1, when it was administered in 2-month-olds. However, administration at 4 months of age did not result in a preventive effect. These findings suggest that the administration of magnolol before the initiation of neuronal loss may result in a protective effect in the hippocampus.</description><subject>Aging - drug effects</subject><subject>Aging - genetics</subject><subject>Aging - pathology</subject><subject>Animals</subject><subject>Biphenyl Compounds - pharmacology</subject><subject>Cell Count</subject><subject>hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - pathology</subject><subject>Lignans - pharmacology</subject><subject>magnolol</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Nerve Degeneration - pathology</subject><subject>Neurites - drug effects</subject><subject>Neurofibrils - drug effects</subject><subject>senescence accelerated mouse</subject><subject>Tissue Embedding</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2P0zAQxSMEYsvCiTuKhIRAKMXjZBLnRlXtB9IWEAtny7HHras0Dk5y4L9fd9NlJS5cZg7zm_dm9JLkNbAl8EJ8avpmycUSqpI_SRaQF1WGHPBpsmA1iKwEFGfJi2HYM8YqxvPnyRmUUAAiLhLzlabgx-D7ndPphbWkx9TbdKO2nW99m7ouHXeUXru-91odetWm6xWkP2jrfHckb6mjQVOnKVtpTS0FNZJJN05T-v52tfkOH14mz6xqB3p16ufJr8uLn-vr7Obb1Zf16ibTFWdjZilHYwWjxhhT2spoa4wwihqiGrBUDeRIKAoUFVrgGqHRRY6sVlSaQuXnybtZtw_-90TDKA8unta2qiM_DbIUiFDX5X9BqPJoAxjBt_-Aez-FLj4hoSjqHAFrHqmPM6WDH4ZAVvbBHVT4I4HJY0YyZiS5kMeMIv3mpDk1BzKP7CmUCFzNQJw6rVrfta6jR2c9VI2L4UjOGErGuGC1ZEV-L38sCKwqa15Epc-z0n4Y1Zb-WqkwOt3Sw1n1XO7XH0Z6p4KkLr8Dhmi5Aw</recordid><startdate>20050901</startdate><enddate>20050901</enddate><creator>Matsui, Nobuaki</creator><creator>Nakashima, Hiroshi</creator><creator>Ushio, Yuki</creator><creator>Tada, Toshimasa</creator><creator>Shirono, Akiko</creator><creator>Fukuyama, Yoshiyasu</creator><creator>Nakade, Kousuke</creator><creator>Zhai, Haifeng</creator><creator>Yasui, Yumiko</creator><creator>Fukuishi, Nobuyuki</creator><creator>Akagi, Reiko</creator><creator>Akagi, Masaaki</creator><general>The Pharmaceutical Society of Japan</general><general>Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20050901</creationdate><title>Neurotrophic Effect of Magnolol in the Hippocampal CA1 Region of Senescence-Accelerated Mice (SAMP1)</title><author>Matsui, Nobuaki ; 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In this study, we investigated the protective effect of magnolol against age-related neuronal loss in the hippocampus using senescence-accelerated mouse (SAMP1). Magnolol (5, 10 mg/kg) was orally administered once a day for 14 d to 2- or 4-month-old mice, and evaluation was carried out when the mice were 4 or 6 months old. The density of neurofibrils decreased with aging in the stratum radiatum of the CA1 region in the hippocampus of SAMP1, not SAMR1. Treatment with magnolol significantly prevented the decrease of neurofibrils in the CA1, when it was administered in 2-month-olds. However, administration at 4 months of age did not result in a preventive effect. These findings suggest that the administration of magnolol before the initiation of neuronal loss may result in a protective effect in the hippocampus.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>16141555</pmid><doi>10.1248/bpb.28.1762</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aging - drug effects Aging - genetics Aging - pathology Animals Biphenyl Compounds - pharmacology Cell Count hippocampus Hippocampus - cytology Hippocampus - drug effects Hippocampus - pathology Lignans - pharmacology magnolol Mice Mice, Inbred Strains Nerve Degeneration - pathology Neurites - drug effects Neurofibrils - drug effects senescence accelerated mouse Tissue Embedding |
title | Neurotrophic Effect of Magnolol in the Hippocampal CA1 Region of Senescence-Accelerated Mice (SAMP1) |
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