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Naringenin attenuates behavioral derangements induced by social defeat stress in mice via inhibition of acetylcholinesterase activity, oxidative stress and release of pro-inflammatory cytokines
The effects of naringenin; a dietary flavonoid, with potent anti-oxidant and anti-inflammatory activities on social defeat stress (SDS)-induced neurobehavioral and biochemical changes were evaluated in mice using resident-intruder paradigm. The intruder male mice were distributed into 6 groups (n = ...
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Published in: | Biomedicine & pharmacotherapy 2018-09, Vol.105, p.714-723 |
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description | The effects of naringenin; a dietary flavonoid, with potent anti-oxidant and anti-inflammatory activities on social defeat stress (SDS)-induced neurobehavioral and biochemical changes were evaluated in mice using resident-intruder paradigm. The intruder male mice were distributed into 6 groups (n = 6). Mice in group 1 (control) received vehicle (3% DMSO, i.p), group 2 (SDS-control) were also given vehicle, groups 3–5 received naringenin (10, 25 and 50 mg/kg, i.p.) while group 6 had ginseng (50 mg/kg, i.p) daily for 14 days. However, 30 min after treatment on day 7, mice in groups 2–6 were exposed to SDS for a period of 10 min confrontation with aggressive counterparts for 7 consecutive days. Neurobehavioral phenotypes: spontaneous motor activity (SMA), memory, anxiety and depression were then evaluated on day 14. Malondialdehyde (MDA), glutathione (GSH), catalase and superoxide dismutase (SOD) were then estimated in the brain tissues. Acetylcholinesterase (AChE) activity and the concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) were also determined. SDS-induced neurobehavioral deficits were significantly (p |
doi_str_mv | 10.1016/j.biopha.2018.06.016 |
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The intruder male mice were distributed into 6 groups (n = 6). Mice in group 1 (control) received vehicle (3% DMSO, i.p), group 2 (SDS-control) were also given vehicle, groups 3–5 received naringenin (10, 25 and 50 mg/kg, i.p.) while group 6 had ginseng (50 mg/kg, i.p) daily for 14 days. However, 30 min after treatment on day 7, mice in groups 2–6 were exposed to SDS for a period of 10 min confrontation with aggressive counterparts for 7 consecutive days. Neurobehavioral phenotypes: spontaneous motor activity (SMA), memory, anxiety and depression were then evaluated on day 14. Malondialdehyde (MDA), glutathione (GSH), catalase and superoxide dismutase (SOD) were then estimated in the brain tissues. Acetylcholinesterase (AChE) activity and the concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) were also determined. SDS-induced neurobehavioral deficits were significantly (p < 0.05) attenuated by naringenin. The increased brain level of MDA (13.00 ± 0.63 μmol/g tissue) relative to vehicle-control (6.50 ± 0.43 μmol/g tissue) was significantly (p < 0.05) reduced to 5.50 ± 0.22 μmol/g tissue by naringenin (50 mg/kg). Mice exposed to SDS had decreased brain GSH level (5.17 ± 0.40 μmol/g tissue) relative to control (11.67 ± 0.84 μmol/g tissue). However, naringenin (50 mg/kg) significantly (p < 0.05) elevated GSH content (13.33 ± 0.88 μmol/g tissue) in the brains of SDS-mice. Moreover, 50 mg/Kg of naringenin (38.13 ± 2.38 ρg/mL) attenuated (p < 0.05) increased TNF-α level when compared with SDS (49.69 ± 2.81 ρg/mL). SDS-induced increase in brain level of IL-1β (236.5 ± 6.92 ρg/mL) was significantly (p < 0.05) reduced by naringenin (219.90 ± 15.25 ρg/mL). Naringenin also elevated antioxidant enzymes and decreased AChE activity in the brains of mice exposed to SDS (p < 0.05). These findings suggest that naringenin attenuates SDS-induced neurobehavioral deficits through inhibition of acetylcholinesterase activity, oxidative stress and release of pro-inflammatory cytokines.]]></description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2018.06.016</identifier><identifier>PMID: 29906750</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Acetylcholinesterase - metabolism ; Animals ; Behavior, Animal - drug effects ; Brain - drug effects ; Brain - enzymology ; Brain - immunology ; Cholinesterase Inhibitors - pharmacology ; Cytokines - secretion ; Flavanones - pharmacology ; Inflammation ; Male ; Motor Activity - drug effects ; Naringenin ; Neurobehavioral deficits ; Oxidative stress ; Oxidative Stress - drug effects ; Proinflammatory cytokines ; Social defeat stress ; Social Isolation - psychology ; Stress, Psychological - enzymology ; Stress, Psychological - immunology ; Stress, Psychological - psychology</subject><ispartof>Biomedicine & pharmacotherapy, 2018-09, Vol.105, p.714-723</ispartof><rights>2018 Elsevier Masson SAS</rights><rights>Copyright © 2018 Elsevier Masson SAS. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-f3af0c304e3a82e28279ab00d4bef42467de62e0d461238eead1eed6d605b85b3</citedby><cites>FETCH-LOGICAL-c428t-f3af0c304e3a82e28279ab00d4bef42467de62e0d461238eead1eed6d605b85b3</cites><orcidid>0000-0001-6586-0421</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29906750$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Umukoro, Solomon</creatorcontrib><creatorcontrib>Kalejaye, Hassanat Adeola</creatorcontrib><creatorcontrib>Ben-Azu, Benneth</creatorcontrib><creatorcontrib>Ajayi, Abayomi M.</creatorcontrib><title>Naringenin attenuates behavioral derangements induced by social defeat stress in mice via inhibition of acetylcholinesterase activity, oxidative stress and release of pro-inflammatory cytokines</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description><![CDATA[The effects of naringenin; a dietary flavonoid, with potent anti-oxidant and anti-inflammatory activities on social defeat stress (SDS)-induced neurobehavioral and biochemical changes were evaluated in mice using resident-intruder paradigm. The intruder male mice were distributed into 6 groups (n = 6). Mice in group 1 (control) received vehicle (3% DMSO, i.p), group 2 (SDS-control) were also given vehicle, groups 3–5 received naringenin (10, 25 and 50 mg/kg, i.p.) while group 6 had ginseng (50 mg/kg, i.p) daily for 14 days. However, 30 min after treatment on day 7, mice in groups 2–6 were exposed to SDS for a period of 10 min confrontation with aggressive counterparts for 7 consecutive days. Neurobehavioral phenotypes: spontaneous motor activity (SMA), memory, anxiety and depression were then evaluated on day 14. Malondialdehyde (MDA), glutathione (GSH), catalase and superoxide dismutase (SOD) were then estimated in the brain tissues. Acetylcholinesterase (AChE) activity and the concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) were also determined. SDS-induced neurobehavioral deficits were significantly (p < 0.05) attenuated by naringenin. The increased brain level of MDA (13.00 ± 0.63 μmol/g tissue) relative to vehicle-control (6.50 ± 0.43 μmol/g tissue) was significantly (p < 0.05) reduced to 5.50 ± 0.22 μmol/g tissue by naringenin (50 mg/kg). Mice exposed to SDS had decreased brain GSH level (5.17 ± 0.40 μmol/g tissue) relative to control (11.67 ± 0.84 μmol/g tissue). However, naringenin (50 mg/kg) significantly (p < 0.05) elevated GSH content (13.33 ± 0.88 μmol/g tissue) in the brains of SDS-mice. Moreover, 50 mg/Kg of naringenin (38.13 ± 2.38 ρg/mL) attenuated (p < 0.05) increased TNF-α level when compared with SDS (49.69 ± 2.81 ρg/mL). SDS-induced increase in brain level of IL-1β (236.5 ± 6.92 ρg/mL) was significantly (p < 0.05) reduced by naringenin (219.90 ± 15.25 ρg/mL). Naringenin also elevated antioxidant enzymes and decreased AChE activity in the brains of mice exposed to SDS (p < 0.05). These findings suggest that naringenin attenuates SDS-induced neurobehavioral deficits through inhibition of acetylcholinesterase activity, oxidative stress and release of pro-inflammatory cytokines.]]></description><subject>Acetylcholinesterase - metabolism</subject><subject>Animals</subject><subject>Behavior, Animal - drug effects</subject><subject>Brain - drug effects</subject><subject>Brain - enzymology</subject><subject>Brain - immunology</subject><subject>Cholinesterase Inhibitors - pharmacology</subject><subject>Cytokines - secretion</subject><subject>Flavanones - pharmacology</subject><subject>Inflammation</subject><subject>Male</subject><subject>Motor Activity - drug effects</subject><subject>Naringenin</subject><subject>Neurobehavioral deficits</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Proinflammatory cytokines</subject><subject>Social defeat stress</subject><subject>Social Isolation - psychology</subject><subject>Stress, Psychological - enzymology</subject><subject>Stress, Psychological - immunology</subject><subject>Stress, Psychological - psychology</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9UcuO1DAQjBCIHRb-ACEfOZCh4ySezAUJrXhJK7jA2erYHaaHxB5sZ0Q-jz_DYXY5crK7uqra7SqK5xVsK6jU6-O2Z3864FZC1W1BbTP4oNhU-xZKBbB7WGxg19ZlXUt5VTyJ8QgAraq7x8WV3O9B7VrYFL8_Y2D3nRw7gSmRmzFRFD0d8Mw-4CgsBcyEiVyKgp2dDVnRLyJ6w3_bA2ESMQWKa19MbEicGfP9wD0n9k74QaChtIzm4Ed2FFM2jZTBxGdOyyvhf7HFXNC9EzorAo200rL8FHzJbhhxmjD5sAizJP9jtXpaPBpwjPTs7rwuvr1_9_XmY3n75cOnm7e3pWlkl8qhxgFMDQ3V2EmSndztsQewTU9DIxu1s6Qk5VpVsu6I0FZEVlkFbd-1fX1dvLz45qf8nPMKeuJoaBzRkZ-jluvn7lsFVaY2F6oJPsZAgz4FnjAsugK9hqeP-hKeXsPToHQGs-zF3YS5n8j-E92nlQlvLgTKe56Zgo6GyeVAOJBJ2nr-_4Q_yuez3g</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Umukoro, Solomon</creator><creator>Kalejaye, Hassanat Adeola</creator><creator>Ben-Azu, Benneth</creator><creator>Ajayi, Abayomi M.</creator><general>Elsevier Masson SAS</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>7X8</scope><orcidid>https://orcid.org/0000-0001-6586-0421</orcidid></search><sort><creationdate>201809</creationdate><title>Naringenin attenuates behavioral derangements induced by social defeat stress in mice via inhibition of acetylcholinesterase activity, oxidative stress and release of pro-inflammatory cytokines</title><author>Umukoro, Solomon ; Kalejaye, Hassanat Adeola ; Ben-Azu, Benneth ; Ajayi, Abayomi M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-f3af0c304e3a82e28279ab00d4bef42467de62e0d461238eead1eed6d605b85b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetylcholinesterase - metabolism</topic><topic>Animals</topic><topic>Behavior, Animal - drug effects</topic><topic>Brain - drug effects</topic><topic>Brain - enzymology</topic><topic>Brain - immunology</topic><topic>Cholinesterase Inhibitors - pharmacology</topic><topic>Cytokines - secretion</topic><topic>Flavanones - pharmacology</topic><topic>Inflammation</topic><topic>Male</topic><topic>Motor Activity - drug effects</topic><topic>Naringenin</topic><topic>Neurobehavioral deficits</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Proinflammatory cytokines</topic><topic>Social defeat stress</topic><topic>Social Isolation - psychology</topic><topic>Stress, Psychological - enzymology</topic><topic>Stress, Psychological - immunology</topic><topic>Stress, Psychological - psychology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Umukoro, Solomon</creatorcontrib><creatorcontrib>Kalejaye, Hassanat Adeola</creatorcontrib><creatorcontrib>Ben-Azu, Benneth</creatorcontrib><creatorcontrib>Ajayi, Abayomi M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biomedicine & pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Umukoro, Solomon</au><au>Kalejaye, Hassanat Adeola</au><au>Ben-Azu, Benneth</au><au>Ajayi, Abayomi M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Naringenin attenuates behavioral derangements induced by social defeat stress in mice via inhibition of acetylcholinesterase activity, oxidative stress and release of pro-inflammatory cytokines</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2018-09</date><risdate>2018</risdate><volume>105</volume><spage>714</spage><epage>723</epage><pages>714-723</pages><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract><![CDATA[The effects of naringenin; a dietary flavonoid, with potent anti-oxidant and anti-inflammatory activities on social defeat stress (SDS)-induced neurobehavioral and biochemical changes were evaluated in mice using resident-intruder paradigm. The intruder male mice were distributed into 6 groups (n = 6). Mice in group 1 (control) received vehicle (3% DMSO, i.p), group 2 (SDS-control) were also given vehicle, groups 3–5 received naringenin (10, 25 and 50 mg/kg, i.p.) while group 6 had ginseng (50 mg/kg, i.p) daily for 14 days. However, 30 min after treatment on day 7, mice in groups 2–6 were exposed to SDS for a period of 10 min confrontation with aggressive counterparts for 7 consecutive days. Neurobehavioral phenotypes: spontaneous motor activity (SMA), memory, anxiety and depression were then evaluated on day 14. Malondialdehyde (MDA), glutathione (GSH), catalase and superoxide dismutase (SOD) were then estimated in the brain tissues. Acetylcholinesterase (AChE) activity and the concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) were also determined. SDS-induced neurobehavioral deficits were significantly (p < 0.05) attenuated by naringenin. The increased brain level of MDA (13.00 ± 0.63 μmol/g tissue) relative to vehicle-control (6.50 ± 0.43 μmol/g tissue) was significantly (p < 0.05) reduced to 5.50 ± 0.22 μmol/g tissue by naringenin (50 mg/kg). Mice exposed to SDS had decreased brain GSH level (5.17 ± 0.40 μmol/g tissue) relative to control (11.67 ± 0.84 μmol/g tissue). However, naringenin (50 mg/kg) significantly (p < 0.05) elevated GSH content (13.33 ± 0.88 μmol/g tissue) in the brains of SDS-mice. Moreover, 50 mg/Kg of naringenin (38.13 ± 2.38 ρg/mL) attenuated (p < 0.05) increased TNF-α level when compared with SDS (49.69 ± 2.81 ρg/mL). SDS-induced increase in brain level of IL-1β (236.5 ± 6.92 ρg/mL) was significantly (p < 0.05) reduced by naringenin (219.90 ± 15.25 ρg/mL). Naringenin also elevated antioxidant enzymes and decreased AChE activity in the brains of mice exposed to SDS (p < 0.05). These findings suggest that naringenin attenuates SDS-induced neurobehavioral deficits through inhibition of acetylcholinesterase activity, oxidative stress and release of pro-inflammatory cytokines.]]></abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>29906750</pmid><doi>10.1016/j.biopha.2018.06.016</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-6586-0421</orcidid></addata></record> |
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subjects | Acetylcholinesterase - metabolism Animals Behavior, Animal - drug effects Brain - drug effects Brain - enzymology Brain - immunology Cholinesterase Inhibitors - pharmacology Cytokines - secretion Flavanones - pharmacology Inflammation Male Motor Activity - drug effects Naringenin Neurobehavioral deficits Oxidative stress Oxidative Stress - drug effects Proinflammatory cytokines Social defeat stress Social Isolation - psychology Stress, Psychological - enzymology Stress, Psychological - immunology Stress, Psychological - psychology |
title | Naringenin attenuates behavioral derangements induced by social defeat stress in mice via inhibition of acetylcholinesterase activity, oxidative stress and release of pro-inflammatory cytokines |
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