Effects of low dose of ethanol on the senescence score, brain function and gene expression in senescence-accelerated mice 8 (SAMP8)
Accumulating epidemiological evidence suggests light to moderate alcohol intake reduces risk of several chronic diseases. However, there is limited information regarding the effects of low alcohol intake in animal studies. This study investigated the effect of low ethanol dosage on senescence-accele...
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| Veröffentlicht in: | Experimental and therapeutic medicine 2017-08, Vol.14 (2), p.1433-1440 |
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| description | Accumulating epidemiological evidence suggests light to moderate alcohol intake reduces risk of several chronic diseases. However, there is limited information regarding the effects of low alcohol intake in animal studies. This study investigated the effect of low ethanol dosage on senescence-accelerated mouse (SAMP8), an animal model of aging and neurodegenaration. Male SAMP8 mice (11 weeks old) had free access to a commercial stock diet with drinking water containing 0, 1 or 2% (v/v) ethanol for 15 weeks. The total grading score of senescence in the 1%-ethanol group was, in large part, the lowest among the three groups. Analysis using the open-field test revealed a significant elevation (+77%, P |
| doi_str_mv | 10.3892/etm.2017.4633 |
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However, there is limited information regarding the effects of low alcohol intake in animal studies. This study investigated the effect of low ethanol dosage on senescence-accelerated mouse (SAMP8), an animal model of aging and neurodegenaration. Male SAMP8 mice (11 weeks old) had free access to a commercial stock diet with drinking water containing 0, 1 or 2% (v/v) ethanol for 15 weeks. The total grading score of senescence in the 1%-ethanol group was, in large part, the lowest among the three groups. Analysis using the open-field test revealed a significant elevation (+77%, P<0.05) in the rearing activity (index of seeking behavior) in the 1%-ethanol group, but not in the 2%-ethanol group. In addition, 2% ethanol elevated spontaneous locomotor activity (+75%, P<0.05), whereas 1% ethanol did not. Scrutiny of serum parameters indicated intake of 1% ethanol significantly decreased serum insulin levels (−13%, P<0.05), whereas 2% did not. Intake of 2% ethanol significantly elevated (2.5-fold, P<0.05) S100a8 mRNA (an inflammatory signal) in the brain, but that of 1% ethanol did not. Intriguingly, 1% ethanol intake remarkably elevated (10-fold, P<0.05) mRNA of brain alcohol dehydrogenase 1 (Adh1), which metabolizes lipid-peroxidation products and is involved in the synthesis of retinoic acid, a neuroprotective factor. Of note, 2%-ethanol intake did not exert this effect. Taken together, intake of 1% ethanol is likely to be beneficial for SAMP8 mice.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2017.4633</identifier><identifier>PMID: 28810607</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Aging ; alcohol dehydrogenase 1 ; Alcohol dehydrogenases ; Animal cognition ; brain ; Brain research ; Chronic diseases ; Consumption ; Dementia ; Drinking water ; Ethanol ; Food ; Gene expression ; Insulin ; Insulin-like growth factors ; Kinases ; Laboratory animals ; Light ; Risk factors ; Rodents ; Senescence ; senescence-accelerated mouse prone 8 ; Studies ; Tumor necrosis factor-TNF ; Ulcers</subject><ispartof>Experimental and therapeutic medicine, 2017-08, Vol.14 (2), p.1433-1440</ispartof><rights>Copyright: © Kimoto et al.</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Kimoto et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c578t-5cc3336a390b9cb3bec3712de4e708e0234684c6ecdb3153aeff0d9c87dc6edc3</citedby><cites>FETCH-LOGICAL-c578t-5cc3336a390b9cb3bec3712de4e708e0234684c6ecdb3153aeff0d9c87dc6edc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5525595/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5525595/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28810607$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kimoto, Akiko</creatorcontrib><creatorcontrib>Izu, Hanae</creatorcontrib><creatorcontrib>Fu, Churan</creatorcontrib><creatorcontrib>Suidasari, Sofya</creatorcontrib><creatorcontrib>Kato, Norihisa</creatorcontrib><title>Effects of low dose of ethanol on the senescence score, brain function and gene expression in senescence-accelerated mice 8 (SAMP8)</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>Accumulating epidemiological evidence suggests light to moderate alcohol intake reduces risk of several chronic diseases. However, there is limited information regarding the effects of low alcohol intake in animal studies. This study investigated the effect of low ethanol dosage on senescence-accelerated mouse (SAMP8), an animal model of aging and neurodegenaration. Male SAMP8 mice (11 weeks old) had free access to a commercial stock diet with drinking water containing 0, 1 or 2% (v/v) ethanol for 15 weeks. The total grading score of senescence in the 1%-ethanol group was, in large part, the lowest among the three groups. Analysis using the open-field test revealed a significant elevation (+77%, P<0.05) in the rearing activity (index of seeking behavior) in the 1%-ethanol group, but not in the 2%-ethanol group. In addition, 2% ethanol elevated spontaneous locomotor activity (+75%, P<0.05), whereas 1% ethanol did not. Scrutiny of serum parameters indicated intake of 1% ethanol significantly decreased serum insulin levels (−13%, P<0.05), whereas 2% did not. Intake of 2% ethanol significantly elevated (2.5-fold, P<0.05) S100a8 mRNA (an inflammatory signal) in the brain, but that of 1% ethanol did not. Intriguingly, 1% ethanol intake remarkably elevated (10-fold, P<0.05) mRNA of brain alcohol dehydrogenase 1 (Adh1), which metabolizes lipid-peroxidation products and is involved in the synthesis of retinoic acid, a neuroprotective factor. Of note, 2%-ethanol intake did not exert this effect. Taken together, intake of 1% ethanol is likely to be beneficial for SAMP8 mice.</description><subject>Aging</subject><subject>alcohol dehydrogenase 1</subject><subject>Alcohol dehydrogenases</subject><subject>Animal cognition</subject><subject>brain</subject><subject>Brain research</subject><subject>Chronic diseases</subject><subject>Consumption</subject><subject>Dementia</subject><subject>Drinking water</subject><subject>Ethanol</subject><subject>Food</subject><subject>Gene expression</subject><subject>Insulin</subject><subject>Insulin-like growth factors</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Light</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Senescence</subject><subject>senescence-accelerated mouse prone 8</subject><subject>Studies</subject><subject>Tumor necrosis factor-TNF</subject><subject>Ulcers</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk2LFDEQhhtR3GXdo1cJiLCCPSadTie5CMMyfsAuCq7nkE5Xz2TpScak24-zf9xqZxxdMXVIUXnqDZW8RfGY0QVXunoJ43ZRUSYXdcP5veKUSV2VjDJx_5BTrdhJcZ7zLcUlGqaUeFicVEox2lB5WvxY9T24MZPYkyF-JV3MMOcwbmyIA4mBjBsgGQJkB8Fh6mKCF6RN1gfST8GNHiEbOrJGiMC3XYKc5xqe_-krrXMwQLIjdGTrUUiRi4_L6w_q-aPiQW-HDOeH_az49Hp1c_m2vHr_5t3l8qp0QqqxFM5xzhvLNW21a3kLjktWdVCDpApoxetG1a4B17WcCW6h72mnnZIdFjvHz4pXe93d1G6xAGFMdjC75Lc2fTfRenP3JPiNWccvRohKCC1Q4OIgkOLnCfJoth6nGwYbIE7ZMF1pTRlTDNGn_6C3cUoBx0NK1wox_LIjtbYDGB_6iPe6WdQsBa2ZlJJJpBb_oTA6wIeMAXqP9TsN5b7BpZhzgv44I6NmNo5B45jZOGY2DvJP_n6YI_3bJgg82wN5hx_t0SRHZnVzXVKMX0I_AdEMynA</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Kimoto, Akiko</creator><creator>Izu, Hanae</creator><creator>Fu, Churan</creator><creator>Suidasari, Sofya</creator><creator>Kato, Norihisa</creator><general>D.A. 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However, there is limited information regarding the effects of low alcohol intake in animal studies. This study investigated the effect of low ethanol dosage on senescence-accelerated mouse (SAMP8), an animal model of aging and neurodegenaration. Male SAMP8 mice (11 weeks old) had free access to a commercial stock diet with drinking water containing 0, 1 or 2% (v/v) ethanol for 15 weeks. The total grading score of senescence in the 1%-ethanol group was, in large part, the lowest among the three groups. Analysis using the open-field test revealed a significant elevation (+77%, P<0.05) in the rearing activity (index of seeking behavior) in the 1%-ethanol group, but not in the 2%-ethanol group. In addition, 2% ethanol elevated spontaneous locomotor activity (+75%, P<0.05), whereas 1% ethanol did not. Scrutiny of serum parameters indicated intake of 1% ethanol significantly decreased serum insulin levels (−13%, P<0.05), whereas 2% did not. Intake of 2% ethanol significantly elevated (2.5-fold, P<0.05) S100a8 mRNA (an inflammatory signal) in the brain, but that of 1% ethanol did not. Intriguingly, 1% ethanol intake remarkably elevated (10-fold, P<0.05) mRNA of brain alcohol dehydrogenase 1 (Adh1), which metabolizes lipid-peroxidation products and is involved in the synthesis of retinoic acid, a neuroprotective factor. Of note, 2%-ethanol intake did not exert this effect. Taken together, intake of 1% ethanol is likely to be beneficial for SAMP8 mice.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28810607</pmid><doi>10.3892/etm.2017.4633</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aging alcohol dehydrogenase 1 Alcohol dehydrogenases Animal cognition brain Brain research Chronic diseases Consumption Dementia Drinking water Ethanol Food Gene expression Insulin Insulin-like growth factors Kinases Laboratory animals Light Risk factors Rodents Senescence senescence-accelerated mouse prone 8 Studies Tumor necrosis factor-TNF Ulcers |
| title | Effects of low dose of ethanol on the senescence score, brain function and gene expression in senescence-accelerated mice 8 (SAMP8) |
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