Catechin Hydrate Ameliorates Redox Imbalance and Limits Inflammatory Response in Focal Cerebral Ischemia
Epidemiologic studies have shown that foods rich in polyphenols, such as flavonoids, can lower the risk of ischemic disease; however, the mechanism of protection has not been clearly investigated. In this study, we hypothesized that pretreatment effect of catechin hydrate (CH) on functional outcome,...
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Veröffentlicht in: | Neurochemical research 2012-08, Vol.37 (8), p.1747-1760 |
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creator | Ashafaq, Mohammad Raza, Syed Shadab Khan, Mohd. Moshahid Ahmad, Ajmal Javed, Hayate Ahmad, Md. Ejaz Tabassum, Rizwana Islam, Farah Siddiqui, M. Saeed Safhi, Mohammed M. Islam, Fakhrul |
description | Epidemiologic studies have shown that foods rich in polyphenols, such as flavonoids, can lower the risk of ischemic disease; however, the mechanism of protection has not been clearly investigated. In this study, we hypothesized that pretreatment effect of catechin hydrate (CH) on functional outcome, neuronal damage and on secondary injuries in the ischemic brain of rats. To test this hypothesis, male Wistar rats were pretreated with CH (20 mg/kg b.wt) for 21 days and then subjected to 2 h middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion. After 2 h MCAO/22 h reperfusion, neurological deficit, infarct sizes, activities of antioxidant enzymes and cytokines level were measured. Immunohistochemistry and western blot were used to analyse the expression of glial fibrillary acidic protein (GFAP), inducible nitric oxide (iNOS) and NF-kB in ischemic brain. The administration of CH showed marked reduction in infarct size, reduced the neurological deficits, suppressed neuronal loss and downregulate the iNOS, GFAP and NF-kB expression in MCAO rats. A significantly depleted activity of antioxidant enzymes and content of glutathione in MCAO group were protected significantly in MCAO group pretreated with CH. Conversely, the elevated level of thiobarbituric acid reactive species and cytokines in MCAO group was attenuated significantly in CH pretreated group when compared with MCAO group. The results indicated that CH protected the brain from damage caused by MCAO, and this effect may be through downregulation of NF-kB expression. |
doi_str_mv | 10.1007/s11064-012-0786-1 |
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Moshahid ; Ahmad, Ajmal ; Javed, Hayate ; Ahmad, Md. Ejaz ; Tabassum, Rizwana ; Islam, Farah ; Siddiqui, M. Saeed ; Safhi, Mohammed M. ; Islam, Fakhrul</creator><creatorcontrib>Ashafaq, Mohammad ; Raza, Syed Shadab ; Khan, Mohd. Moshahid ; Ahmad, Ajmal ; Javed, Hayate ; Ahmad, Md. Ejaz ; Tabassum, Rizwana ; Islam, Farah ; Siddiqui, M. Saeed ; Safhi, Mohammed M. ; Islam, Fakhrul</creatorcontrib><description>Epidemiologic studies have shown that foods rich in polyphenols, such as flavonoids, can lower the risk of ischemic disease; however, the mechanism of protection has not been clearly investigated. In this study, we hypothesized that pretreatment effect of catechin hydrate (CH) on functional outcome, neuronal damage and on secondary injuries in the ischemic brain of rats. To test this hypothesis, male Wistar rats were pretreated with CH (20 mg/kg b.wt) for 21 days and then subjected to 2 h middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion. After 2 h MCAO/22 h reperfusion, neurological deficit, infarct sizes, activities of antioxidant enzymes and cytokines level were measured. Immunohistochemistry and western blot were used to analyse the expression of glial fibrillary acidic protein (GFAP), inducible nitric oxide (iNOS) and NF-kB in ischemic brain. The administration of CH showed marked reduction in infarct size, reduced the neurological deficits, suppressed neuronal loss and downregulate the iNOS, GFAP and NF-kB expression in MCAO rats. A significantly depleted activity of antioxidant enzymes and content of glutathione in MCAO group were protected significantly in MCAO group pretreated with CH. Conversely, the elevated level of thiobarbituric acid reactive species and cytokines in MCAO group was attenuated significantly in CH pretreated group when compared with MCAO group. The results indicated that CH protected the brain from damage caused by MCAO, and this effect may be through downregulation of NF-kB expression.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-012-0786-1</identifier><identifier>PMID: 22570178</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Antioxidants ; Antioxidants - metabolism ; Behavior, Animal - drug effects ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Brain - drug effects ; Brain injury ; Brain Ischemia - metabolism ; Catechin ; Catechin - pharmacology ; Cell Biology ; Cerebral blood flow ; Cerebral Infarction - pathology ; Cerebral Infarction - prevention & control ; Cytokines ; Enzymes ; Flavonoids ; Food ; Glial fibrillary acidic protein ; Glial Fibrillary Acidic Protein - biosynthesis ; Glutathione ; Glutathione - metabolism ; Infarction, Middle Cerebral Artery - physiopathology ; Ischemia ; Male ; Neurochemistry ; Neurological diseases ; Neurology ; Neurosciences ; NF- Kappa B protein ; NF-kappa B - biosynthesis ; Nitric Oxide Synthase Type II - biosynthesis ; Nitric-oxide synthase ; Original Paper ; Oxidation-Reduction ; Rats ; Rats, Wistar ; Reperfusion ; Reperfusion Injury - physiopathology ; Reperfusion Injury - prevention & control ; Risk factors ; thiobarbituric acid ; Thiobarbituric Acid Reactive Substances - metabolism ; Western blotting</subject><ispartof>Neurochemical research, 2012-08, Vol.37 (8), p.1747-1760</ispartof><rights>Springer Science+Business Media, LLC 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-4b9ce57002d3d5d944b5517474df2526ddfb672b340f78de424b1a2bf85f7c113</citedby><cites>FETCH-LOGICAL-c405t-4b9ce57002d3d5d944b5517474df2526ddfb672b340f78de424b1a2bf85f7c113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-012-0786-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-012-0786-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22570178$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ashafaq, Mohammad</creatorcontrib><creatorcontrib>Raza, Syed Shadab</creatorcontrib><creatorcontrib>Khan, Mohd. Moshahid</creatorcontrib><creatorcontrib>Ahmad, Ajmal</creatorcontrib><creatorcontrib>Javed, Hayate</creatorcontrib><creatorcontrib>Ahmad, Md. Ejaz</creatorcontrib><creatorcontrib>Tabassum, Rizwana</creatorcontrib><creatorcontrib>Islam, Farah</creatorcontrib><creatorcontrib>Siddiqui, M. Saeed</creatorcontrib><creatorcontrib>Safhi, Mohammed M.</creatorcontrib><creatorcontrib>Islam, Fakhrul</creatorcontrib><title>Catechin Hydrate Ameliorates Redox Imbalance and Limits Inflammatory Response in Focal Cerebral Ischemia</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>Epidemiologic studies have shown that foods rich in polyphenols, such as flavonoids, can lower the risk of ischemic disease; however, the mechanism of protection has not been clearly investigated. In this study, we hypothesized that pretreatment effect of catechin hydrate (CH) on functional outcome, neuronal damage and on secondary injuries in the ischemic brain of rats. To test this hypothesis, male Wistar rats were pretreated with CH (20 mg/kg b.wt) for 21 days and then subjected to 2 h middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion. After 2 h MCAO/22 h reperfusion, neurological deficit, infarct sizes, activities of antioxidant enzymes and cytokines level were measured. Immunohistochemistry and western blot were used to analyse the expression of glial fibrillary acidic protein (GFAP), inducible nitric oxide (iNOS) and NF-kB in ischemic brain. The administration of CH showed marked reduction in infarct size, reduced the neurological deficits, suppressed neuronal loss and downregulate the iNOS, GFAP and NF-kB expression in MCAO rats. A significantly depleted activity of antioxidant enzymes and content of glutathione in MCAO group were protected significantly in MCAO group pretreated with CH. Conversely, the elevated level of thiobarbituric acid reactive species and cytokines in MCAO group was attenuated significantly in CH pretreated group when compared with MCAO group. The results indicated that CH protected the brain from damage caused by MCAO, and this effect may be through downregulation of NF-kB expression.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Behavior, Animal - drug effects</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Brain - drug effects</subject><subject>Brain injury</subject><subject>Brain Ischemia - metabolism</subject><subject>Catechin</subject><subject>Catechin - pharmacology</subject><subject>Cell Biology</subject><subject>Cerebral blood flow</subject><subject>Cerebral Infarction - pathology</subject><subject>Cerebral Infarction - prevention & control</subject><subject>Cytokines</subject><subject>Enzymes</subject><subject>Flavonoids</subject><subject>Food</subject><subject>Glial fibrillary acidic protein</subject><subject>Glial Fibrillary Acidic Protein - biosynthesis</subject><subject>Glutathione</subject><subject>Glutathione - metabolism</subject><subject>Infarction, Middle Cerebral Artery - physiopathology</subject><subject>Ischemia</subject><subject>Male</subject><subject>Neurochemistry</subject><subject>Neurological diseases</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>NF- Kappa B protein</subject><subject>NF-kappa B - biosynthesis</subject><subject>Nitric Oxide Synthase Type II - biosynthesis</subject><subject>Nitric-oxide synthase</subject><subject>Original Paper</subject><subject>Oxidation-Reduction</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Risk factors</subject><subject>thiobarbituric acid</subject><subject>Thiobarbituric Acid Reactive Substances - metabolism</subject><subject>Western blotting</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kV9LwzAUxYMobk4_gC8S8MWXapKmTfs4hnODgSD6XPLn1nU0zUw6cN_elE0RQQjkwv3dc09yELqm5J4SIh4CpSTnCaEsIaLIE3qCxjQTaZKXJD1FY5LGbkpLMkIXIWwIiVOMnqMRY5kgVBRjtJ7JHvS66fBib3ys8dRC27ihDPgFjPvES6tkKzsNWHYGrxrb9AEvu7qV1sre-X3kwtZ1AXDUmTstWzwDD8rHYhn0GmwjL9FZLdsAV8d7gt7mj6-zRbJ6flrOpqtEc5L1CVelhmiOMJOazJScqyyjggtuapax3Jha5YKplJNaFAY444pKpuoiq4WmNJ2gu4Pu1ruPHYS-sk3Q0MYHgNuFihJWxFOWeURv_6Abt_NddDdQTPAi52mk6IHS3oXgoa62vrHS7yNUDTFUhxiqGEM1xFANJm6OyjtlwfxMfP97BNgBCLHVvYP_vfo_1S81MpGZ</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>Ashafaq, Mohammad</creator><creator>Raza, Syed Shadab</creator><creator>Khan, Mohd. 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Moshahid ; Ahmad, Ajmal ; Javed, Hayate ; Ahmad, Md. Ejaz ; Tabassum, Rizwana ; Islam, Farah ; Siddiqui, M. 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Moshahid</au><au>Ahmad, Ajmal</au><au>Javed, Hayate</au><au>Ahmad, Md. Ejaz</au><au>Tabassum, Rizwana</au><au>Islam, Farah</au><au>Siddiqui, M. Saeed</au><au>Safhi, Mohammed M.</au><au>Islam, Fakhrul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Catechin Hydrate Ameliorates Redox Imbalance and Limits Inflammatory Response in Focal Cerebral Ischemia</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>37</volume><issue>8</issue><spage>1747</spage><epage>1760</epage><pages>1747-1760</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Epidemiologic studies have shown that foods rich in polyphenols, such as flavonoids, can lower the risk of ischemic disease; however, the mechanism of protection has not been clearly investigated. In this study, we hypothesized that pretreatment effect of catechin hydrate (CH) on functional outcome, neuronal damage and on secondary injuries in the ischemic brain of rats. To test this hypothesis, male Wistar rats were pretreated with CH (20 mg/kg b.wt) for 21 days and then subjected to 2 h middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion. After 2 h MCAO/22 h reperfusion, neurological deficit, infarct sizes, activities of antioxidant enzymes and cytokines level were measured. Immunohistochemistry and western blot were used to analyse the expression of glial fibrillary acidic protein (GFAP), inducible nitric oxide (iNOS) and NF-kB in ischemic brain. The administration of CH showed marked reduction in infarct size, reduced the neurological deficits, suppressed neuronal loss and downregulate the iNOS, GFAP and NF-kB expression in MCAO rats. A significantly depleted activity of antioxidant enzymes and content of glutathione in MCAO group were protected significantly in MCAO group pretreated with CH. Conversely, the elevated level of thiobarbituric acid reactive species and cytokines in MCAO group was attenuated significantly in CH pretreated group when compared with MCAO group. The results indicated that CH protected the brain from damage caused by MCAO, and this effect may be through downregulation of NF-kB expression.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22570178</pmid><doi>10.1007/s11064-012-0786-1</doi><tpages>14</tpages></addata></record> |
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subjects | Animals Antioxidants Antioxidants - metabolism Behavior, Animal - drug effects Biochemistry Biomedical and Life Sciences Biomedicine Brain Brain - drug effects Brain injury Brain Ischemia - metabolism Catechin Catechin - pharmacology Cell Biology Cerebral blood flow Cerebral Infarction - pathology Cerebral Infarction - prevention & control Cytokines Enzymes Flavonoids Food Glial fibrillary acidic protein Glial Fibrillary Acidic Protein - biosynthesis Glutathione Glutathione - metabolism Infarction, Middle Cerebral Artery - physiopathology Ischemia Male Neurochemistry Neurological diseases Neurology Neurosciences NF- Kappa B protein NF-kappa B - biosynthesis Nitric Oxide Synthase Type II - biosynthesis Nitric-oxide synthase Original Paper Oxidation-Reduction Rats Rats, Wistar Reperfusion Reperfusion Injury - physiopathology Reperfusion Injury - prevention & control Risk factors thiobarbituric acid Thiobarbituric Acid Reactive Substances - metabolism Western blotting |
title | Catechin Hydrate Ameliorates Redox Imbalance and Limits Inflammatory Response in Focal Cerebral Ischemia |
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