Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats
Alzheimer’s disease is a devastating neurodegenerative disorder, the most common among the dementing illnesses. Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cyto...
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| Veröffentlicht in: | Journal of Clinical Biochemistry and Nutrition 2012, Vol.50(3), pp.241-244 |
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| creator | Pitchaimani, Vigneshwaran Arumugam, Somasundaram Thandavarayan, Rajarajan A. Thiyagarajan, Manisenthilkumar K. Aiyalu, Rajasekaran Sreedhar, Remya Nakamura, Takashi Watanabe, Kenichi |
| description | Alzheimer’s disease is a devastating neurodegenerative disorder, the most common among the dementing illnesses. Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cytokines and increasing the anti apoptotic protein such as Bcl-2 in neuronal cell culture. The low concentration acetaminophen improved the facilitation to find the hidden platform in Morris Water Maze Test. Also some data suggest that acetaminophen could contribute in neurodegeneration. The present study was aimed to evaluate the effect of acetaminophen against colchicine induced cognitive impairment and oxidative stress in wistar rats. The cognitive learning and memory behaviour was assessed using step through passive avoidance paradigm and acetylcholine esterase activity. The parameters of oxidative stress were assessed by measuring the malondialdehyde, reduced glutathione and catalase levels in the whole brain homogenates. There was a significant memory improvement in the rats received acetaminophen treatment and it has also decreased the acetylcholine esterase enzyme level, confirming its nootropic activity. Acetaminophen neither increases nor decreases the reduced glutathione and catalase in the whole brain homogenates, showing that acetaminophen is devoid of any adverse effect on brain antioxidant defense system. |
| doi_str_mv | 10.3164/jcbn.11-73 |
| format | Article |
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Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cytokines and increasing the anti apoptotic protein such as Bcl-2 in neuronal cell culture. The low concentration acetaminophen improved the facilitation to find the hidden platform in Morris Water Maze Test. Also some data suggest that acetaminophen could contribute in neurodegeneration. The present study was aimed to evaluate the effect of acetaminophen against colchicine induced cognitive impairment and oxidative stress in wistar rats. The cognitive learning and memory behaviour was assessed using step through passive avoidance paradigm and acetylcholine esterase activity. The parameters of oxidative stress were assessed by measuring the malondialdehyde, reduced glutathione and catalase levels in the whole brain homogenates. There was a significant memory improvement in the rats received acetaminophen treatment and it has also decreased the acetylcholine esterase enzyme level, confirming its nootropic activity. Acetaminophen neither increases nor decreases the reduced glutathione and catalase in the whole brain homogenates, showing that acetaminophen is devoid of any adverse effect on brain antioxidant defense system.</description><identifier>ISSN: 0912-0009</identifier><identifier>EISSN: 1880-5086</identifier><identifier>DOI: 10.3164/jcbn.11-73</identifier><identifier>PMID: 22573928</identifier><language>eng</language><publisher>Japan: SOCIETY FOR FREE RADICAL RESEARCH JAPAN</publisher><subject>Acetaminophen ; Acetylcholine ; Alzheimer's disease ; Antioxidants ; Apoptosis ; Bcl-2 protein ; Brain ; Caenorhabditis elegans ; Catalase ; Cell culture ; Cognitive ability ; Colchicine ; Dopamine ; Enzymes ; esterase ; Glutathione ; Learning and memory ; Malondialdehyde ; Memory ; Neurodegenerative diseases ; Original ; Oxidative stress</subject><ispartof>Journal of Clinical Biochemistry and Nutrition, 2012, Vol.50(3), pp.241-244</ispartof><rights>2012 by The Editorial Secretariat of JCBN</rights><rights>Copyright Japan Science and Technology Agency 2012</rights><rights>Copyright © 2012 JCBN 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c687t-b84ed9908d125e1bcc4fab56eb5c138ad03ce3d9f6efaa3e4edad5ca44bf278c3</citedby><cites>FETCH-LOGICAL-c687t-b84ed9908d125e1bcc4fab56eb5c138ad03ce3d9f6efaa3e4edad5ca44bf278c3</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/PMC3334379/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3334379/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,1881,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22573928$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pitchaimani, Vigneshwaran</creatorcontrib><creatorcontrib>Arumugam, Somasundaram</creatorcontrib><creatorcontrib>Thandavarayan, Rajarajan A.</creatorcontrib><creatorcontrib>Thiyagarajan, Manisenthilkumar K.</creatorcontrib><creatorcontrib>Aiyalu, Rajasekaran</creatorcontrib><creatorcontrib>Sreedhar, Remya</creatorcontrib><creatorcontrib>Nakamura, Takashi</creatorcontrib><creatorcontrib>Watanabe, Kenichi</creatorcontrib><title>Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats</title><title>Journal of Clinical Biochemistry and Nutrition</title><addtitle>J. Clin. Biochem. Nutr.</addtitle><description>Alzheimer’s disease is a devastating neurodegenerative disorder, the most common among the dementing illnesses. Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cytokines and increasing the anti apoptotic protein such as Bcl-2 in neuronal cell culture. The low concentration acetaminophen improved the facilitation to find the hidden platform in Morris Water Maze Test. Also some data suggest that acetaminophen could contribute in neurodegeneration. The present study was aimed to evaluate the effect of acetaminophen against colchicine induced cognitive impairment and oxidative stress in wistar rats. The cognitive learning and memory behaviour was assessed using step through passive avoidance paradigm and acetylcholine esterase activity. The parameters of oxidative stress were assessed by measuring the malondialdehyde, reduced glutathione and catalase levels in the whole brain homogenates. There was a significant memory improvement in the rats received acetaminophen treatment and it has also decreased the acetylcholine esterase enzyme level, confirming its nootropic activity. Acetaminophen neither increases nor decreases the reduced glutathione and catalase in the whole brain homogenates, showing that acetaminophen is devoid of any adverse effect on brain antioxidant defense system.</description><subject>Acetaminophen</subject><subject>Acetylcholine</subject><subject>Alzheimer's disease</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Bcl-2 protein</subject><subject>Brain</subject><subject>Caenorhabditis elegans</subject><subject>Catalase</subject><subject>Cell culture</subject><subject>Cognitive ability</subject><subject>Colchicine</subject><subject>Dopamine</subject><subject>Enzymes</subject><subject>esterase</subject><subject>Glutathione</subject><subject>Learning and memory</subject><subject>Malondialdehyde</subject><subject>Memory</subject><subject>Neurodegenerative diseases</subject><subject>Original</subject><subject>Oxidative stress</subject><issn>0912-0009</issn><issn>1880-5086</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqFkUtv1DAQgC1ERbeFCz8AReKCkFL8SuJcEKiigFSVC5w4WBNnsutVYgfbqdR_j9MtK-DSi23NfP40D0JeMnohWC3f7U3nLhgrG_GEbJhStKyoqp-SDW0ZLyml7Sk5i3FPqayrWj4jp5xXjWi52pCfN96n4GdrCjDJ3tp0V_ghvzHBZJ2fd-gK2IJ1MRXGj2ZnjXVYWNcvBvsc2jqb_-XINIMNE7qUk0WAFJ-TkwHGiC8e7nPy4-rT98sv5fW3z18vP16XplZNKjslsW9bqnrGK2SdMXKArqqxqwwTCnoqDIq-HWocAARmGvrKgJTdwBtlxDl5f_DOSzdhb3IJAUY9BztBuNMerP434-xOb_2tFkJI0bRZ8OZBEPyvBWPSk40GxxEc-iVqxlWeaEabx1HKeCOV4CKjr_9D934JLk9CMyk5p1SpVfj2QJngYww4HOtmVK_r1et6NWO6WZWv_u70iP7ZZwY-HIB9TLDFIwAhWTPiwVVl8XrcO48ps4Og0YnfkG-7TQ</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>Pitchaimani, Vigneshwaran</creator><creator>Arumugam, Somasundaram</creator><creator>Thandavarayan, Rajarajan A.</creator><creator>Thiyagarajan, Manisenthilkumar K.</creator><creator>Aiyalu, Rajasekaran</creator><creator>Sreedhar, Remya</creator><creator>Nakamura, Takashi</creator><creator>Watanabe, Kenichi</creator><general>SOCIETY FOR FREE RADICAL RESEARCH JAPAN</general><general>Japan Science and Technology Agency</general><general>the Society for Free Radical Research Japan</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120501</creationdate><title>Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats</title><author>Pitchaimani, Vigneshwaran ; Arumugam, Somasundaram ; Thandavarayan, Rajarajan A. ; Thiyagarajan, Manisenthilkumar K. ; Aiyalu, Rajasekaran ; Sreedhar, Remya ; Nakamura, Takashi ; Watanabe, Kenichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c687t-b84ed9908d125e1bcc4fab56eb5c138ad03ce3d9f6efaa3e4edad5ca44bf278c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acetaminophen</topic><topic>Acetylcholine</topic><topic>Alzheimer's disease</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Bcl-2 protein</topic><topic>Brain</topic><topic>Caenorhabditis elegans</topic><topic>Catalase</topic><topic>Cell culture</topic><topic>Cognitive ability</topic><topic>Colchicine</topic><topic>Dopamine</topic><topic>Enzymes</topic><topic>esterase</topic><topic>Glutathione</topic><topic>Learning and memory</topic><topic>Malondialdehyde</topic><topic>Memory</topic><topic>Neurodegenerative diseases</topic><topic>Original</topic><topic>Oxidative stress</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pitchaimani, Vigneshwaran</creatorcontrib><creatorcontrib>Arumugam, Somasundaram</creatorcontrib><creatorcontrib>Thandavarayan, Rajarajan A.</creatorcontrib><creatorcontrib>Thiyagarajan, Manisenthilkumar K.</creatorcontrib><creatorcontrib>Aiyalu, Rajasekaran</creatorcontrib><creatorcontrib>Sreedhar, Remya</creatorcontrib><creatorcontrib>Nakamura, Takashi</creatorcontrib><creatorcontrib>Watanabe, Kenichi</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of Clinical Biochemistry and Nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pitchaimani, Vigneshwaran</au><au>Arumugam, Somasundaram</au><au>Thandavarayan, Rajarajan A.</au><au>Thiyagarajan, Manisenthilkumar K.</au><au>Aiyalu, Rajasekaran</au><au>Sreedhar, Remya</au><au>Nakamura, Takashi</au><au>Watanabe, Kenichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats</atitle><jtitle>Journal of Clinical Biochemistry and Nutrition</jtitle><addtitle>J. Clin. Biochem. Nutr.</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>50</volume><issue>3</issue><spage>241</spage><epage>244</epage><pages>241-244</pages><issn>0912-0009</issn><eissn>1880-5086</eissn><abstract>Alzheimer’s disease is a devastating neurodegenerative disorder, the most common among the dementing illnesses. Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cytokines and increasing the anti apoptotic protein such as Bcl-2 in neuronal cell culture. The low concentration acetaminophen improved the facilitation to find the hidden platform in Morris Water Maze Test. Also some data suggest that acetaminophen could contribute in neurodegeneration. The present study was aimed to evaluate the effect of acetaminophen against colchicine induced cognitive impairment and oxidative stress in wistar rats. The cognitive learning and memory behaviour was assessed using step through passive avoidance paradigm and acetylcholine esterase activity. The parameters of oxidative stress were assessed by measuring the malondialdehyde, reduced glutathione and catalase levels in the whole brain homogenates. There was a significant memory improvement in the rats received acetaminophen treatment and it has also decreased the acetylcholine esterase enzyme level, confirming its nootropic activity. Acetaminophen neither increases nor decreases the reduced glutathione and catalase in the whole brain homogenates, showing that acetaminophen is devoid of any adverse effect on brain antioxidant defense system.</abstract><cop>Japan</cop><pub>SOCIETY FOR FREE RADICAL RESEARCH JAPAN</pub><pmid>22573928</pmid><doi>10.3164/jcbn.11-73</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of Clinical Biochemistry and Nutrition, 2012, Vol.50(3), pp.241-244 |
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| language | eng |
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| source | J-STAGE (Japan Science & Technology Information Aggregator, Electronic) Freely Available Titles - Japanese; PubMed Central (Training); EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | Acetaminophen Acetylcholine Alzheimer's disease Antioxidants Apoptosis Bcl-2 protein Brain Caenorhabditis elegans Catalase Cell culture Cognitive ability Colchicine Dopamine Enzymes esterase Glutathione Learning and memory Malondialdehyde Memory Neurodegenerative diseases Original Oxidative stress |
| title | Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats |
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