Antioxidant and anti-inflammatory effects of hesperidin methyl chalcone in experimental ulcerative colitis
Neutrophil infiltration, pro-inflammatory cytokines, and reactive oxygen species (ROS) production have been implicated in development and progression of ulcerative colitis (UC), an inflammatory bowel disease (IBD) characterized by ulcerating inflammation of the mucosal layer generally restricted to...
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description | Neutrophil infiltration, pro-inflammatory cytokines, and reactive oxygen species (ROS) production have been implicated in development and progression of ulcerative colitis (UC), an inflammatory bowel disease (IBD) characterized by ulcerating inflammation of the mucosal layer generally restricted to the colon. The side effects, safety and human intolerance are limitations of the currently approved treatments for UC. Hesperidin methyl chalcone (HMC) is a flavonoid used to treat chronic venous disease, which shows anti-inflammatory, analgesic, and antioxidant properties in pre-clinical studies, however, its effects on colitis have never been described. Therefore, we aimed to evaluate the protective effects of HMC in a mouse model of acetic acid-induced colitis. Treatment with HMC significantly reduced neutrophil infiltration, edema, colon shortening, macro and microscopic damages induced by intracolonic administration of acetic acid. The improvement of colitis after HMC treatment is related to the increase in colon antioxidant status, and the inhibition of pro-inflammatory cytokines TNF-α, IL-6, IL-1β, and IL-33 in the colon. We observed, moreover, that HMC inhibited NF-κB activation in the colon, which might explain the reduction of the cytokines we observed. Finally, these results demonstrate a novel applicability of HMC to increase antioxidant response and reduce inflammation during acetic acid-induced colitis suggesting it as a promising therapeutic approach for the treatment of ulcerative colitis.
•Methylation of hesperidin produces hesperidin methyl chalcone (HMC).•HMC inhibited neutrophil infiltration, edema and colon shortening in mouse colitis.•HMC also inhibited macroscopic and microscopic damages in colitis.•HMC reduced oxidative stress, cytokine production and NF-κB activation.•This is the first study demonstrating that HMC treats experimental ulcerative colitis. |
doi_str_mv | 10.1016/j.cbi.2020.109315 |
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•Methylation of hesperidin produces hesperidin methyl chalcone (HMC).•HMC inhibited neutrophil infiltration, edema and colon shortening in mouse colitis.•HMC also inhibited macroscopic and microscopic damages in colitis.•HMC reduced oxidative stress, cytokine production and NF-κB activation.•This is the first study demonstrating that HMC treats experimental ulcerative colitis.</description><identifier>ISSN: 0009-2797</identifier><identifier>EISSN: 1872-7786</identifier><identifier>DOI: 10.1016/j.cbi.2020.109315</identifier><identifier>PMID: 33171134</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Chalcones - pharmacology ; Chalcones - therapeutic use ; Colitis, Ulcerative - complications ; Colitis, Ulcerative - drug therapy ; Colitis, Ulcerative - immunology ; Colitis, Ulcerative - metabolism ; Colon - drug effects ; Colon - pathology ; Cytokines - biosynthesis ; Disease Models, Animal ; Edema - complications ; Hesperidin - analogs & derivatives ; Hesperidin - pharmacology ; Hesperidin - therapeutic use ; Hesperidin methyl chalcone ; Inflammation ; Male ; Mice ; Neutrophil Infiltration - drug effects ; NF-kappa B - metabolism ; Oxidative stress ; Oxidative Stress - drug effects ; Ulcerative colitis</subject><ispartof>Chemico-biological interactions, 2021-01, Vol.333, p.109315-109315, Article 109315</ispartof><rights>2020</rights><rights>Copyright © 2020. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-b7edbdf52d4dc8e38441579d378bd8bea42da702993997966ce2ed7db661672b3</citedby><cites>FETCH-LOGICAL-c396t-b7edbdf52d4dc8e38441579d378bd8bea42da702993997966ce2ed7db661672b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cbi.2020.109315$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33171134$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guazelli, Carla F.S.</creatorcontrib><creatorcontrib>Fattori, Victor</creatorcontrib><creatorcontrib>Ferraz, Camila R.</creatorcontrib><creatorcontrib>Borghi, Sergio M.</creatorcontrib><creatorcontrib>Casagrande, Rubia</creatorcontrib><creatorcontrib>Baracat, Marcela M.</creatorcontrib><creatorcontrib>Verri, Waldiceu A.</creatorcontrib><title>Antioxidant and anti-inflammatory effects of hesperidin methyl chalcone in experimental ulcerative colitis</title><title>Chemico-biological interactions</title><addtitle>Chem Biol Interact</addtitle><description>Neutrophil infiltration, pro-inflammatory cytokines, and reactive oxygen species (ROS) production have been implicated in development and progression of ulcerative colitis (UC), an inflammatory bowel disease (IBD) characterized by ulcerating inflammation of the mucosal layer generally restricted to the colon. The side effects, safety and human intolerance are limitations of the currently approved treatments for UC. Hesperidin methyl chalcone (HMC) is a flavonoid used to treat chronic venous disease, which shows anti-inflammatory, analgesic, and antioxidant properties in pre-clinical studies, however, its effects on colitis have never been described. Therefore, we aimed to evaluate the protective effects of HMC in a mouse model of acetic acid-induced colitis. Treatment with HMC significantly reduced neutrophil infiltration, edema, colon shortening, macro and microscopic damages induced by intracolonic administration of acetic acid. The improvement of colitis after HMC treatment is related to the increase in colon antioxidant status, and the inhibition of pro-inflammatory cytokines TNF-α, IL-6, IL-1β, and IL-33 in the colon. We observed, moreover, that HMC inhibited NF-κB activation in the colon, which might explain the reduction of the cytokines we observed. Finally, these results demonstrate a novel applicability of HMC to increase antioxidant response and reduce inflammation during acetic acid-induced colitis suggesting it as a promising therapeutic approach for the treatment of ulcerative colitis.
•Methylation of hesperidin produces hesperidin methyl chalcone (HMC).•HMC inhibited neutrophil infiltration, edema and colon shortening in mouse colitis.•HMC also inhibited macroscopic and microscopic damages in colitis.•HMC reduced oxidative stress, cytokine production and NF-κB activation.•This is the first study demonstrating that HMC treats experimental ulcerative colitis.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Chalcones - pharmacology</subject><subject>Chalcones - therapeutic use</subject><subject>Colitis, Ulcerative - complications</subject><subject>Colitis, Ulcerative - drug therapy</subject><subject>Colitis, Ulcerative - immunology</subject><subject>Colitis, Ulcerative - metabolism</subject><subject>Colon - drug effects</subject><subject>Colon - pathology</subject><subject>Cytokines - biosynthesis</subject><subject>Disease Models, Animal</subject><subject>Edema - complications</subject><subject>Hesperidin - analogs & derivatives</subject><subject>Hesperidin - pharmacology</subject><subject>Hesperidin - therapeutic use</subject><subject>Hesperidin methyl chalcone</subject><subject>Inflammation</subject><subject>Male</subject><subject>Mice</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>NF-kappa B - metabolism</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Ulcerative colitis</subject><issn>0009-2797</issn><issn>1872-7786</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9rGzEQxUVJqZ20H6CXomMu6-rPWlrRkwlJGgj0kp6FVprFMlrJlWQTf_vIOO2xh2GYmTcP3g-hr5SsKKHi-25lR79ihJ1nxen6A1rSQbJOykFcoSUhRHVMKrlA16Xs2khYTz6hBedUUsr7JdptYvXp1TsTKzbRtaq-83EKZp5NTfmEYZrA1oLThLdQ9pC98xHPULengO3WBJsi4LaC1_NxhlhNwIdgIZvqj4BtCr768hl9nEwo8OW936DfD_cvdz-751-PT3eb585yJWo3SnCjm9bM9c4OwIe-p2upHJfD6IYRTM-ckYQpxZWSSggLDJx0oxBUSDbyG3R78d3n9OcAperZFwshmAjpUDTr10qwXjDepPQitTmVkmHS-xbA5JOmRJ8R651uiPUZsb4gbj_f3u0P4wzu38dfpk3w4yKAFvLoIetiPUQLzucGUrvk_2P_BpJojhI</recordid><startdate>20210105</startdate><enddate>20210105</enddate><creator>Guazelli, Carla F.S.</creator><creator>Fattori, Victor</creator><creator>Ferraz, Camila R.</creator><creator>Borghi, Sergio M.</creator><creator>Casagrande, Rubia</creator><creator>Baracat, Marcela M.</creator><creator>Verri, Waldiceu A.</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><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></search><sort><creationdate>20210105</creationdate><title>Antioxidant and anti-inflammatory effects of hesperidin methyl chalcone in experimental ulcerative colitis</title><author>Guazelli, Carla F.S. ; Fattori, Victor ; Ferraz, Camila R. ; Borghi, Sergio M. ; Casagrande, Rubia ; Baracat, Marcela M. ; Verri, Waldiceu A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-b7edbdf52d4dc8e38441579d378bd8bea42da702993997966ce2ed7db661672b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Chalcones - pharmacology</topic><topic>Chalcones - therapeutic use</topic><topic>Colitis, Ulcerative - complications</topic><topic>Colitis, Ulcerative - drug therapy</topic><topic>Colitis, Ulcerative - immunology</topic><topic>Colitis, Ulcerative - metabolism</topic><topic>Colon - drug effects</topic><topic>Colon - pathology</topic><topic>Cytokines - biosynthesis</topic><topic>Disease Models, Animal</topic><topic>Edema - complications</topic><topic>Hesperidin - analogs & derivatives</topic><topic>Hesperidin - pharmacology</topic><topic>Hesperidin - therapeutic use</topic><topic>Hesperidin methyl chalcone</topic><topic>Inflammation</topic><topic>Male</topic><topic>Mice</topic><topic>Neutrophil Infiltration - drug effects</topic><topic>NF-kappa B - metabolism</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Ulcerative colitis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guazelli, Carla F.S.</creatorcontrib><creatorcontrib>Fattori, Victor</creatorcontrib><creatorcontrib>Ferraz, Camila R.</creatorcontrib><creatorcontrib>Borghi, Sergio M.</creatorcontrib><creatorcontrib>Casagrande, Rubia</creatorcontrib><creatorcontrib>Baracat, Marcela M.</creatorcontrib><creatorcontrib>Verri, Waldiceu A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Chemico-biological interactions</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guazelli, Carla F.S.</au><au>Fattori, Victor</au><au>Ferraz, Camila R.</au><au>Borghi, Sergio M.</au><au>Casagrande, Rubia</au><au>Baracat, Marcela M.</au><au>Verri, Waldiceu A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antioxidant and anti-inflammatory effects of hesperidin methyl chalcone in experimental ulcerative colitis</atitle><jtitle>Chemico-biological interactions</jtitle><addtitle>Chem Biol Interact</addtitle><date>2021-01-05</date><risdate>2021</risdate><volume>333</volume><spage>109315</spage><epage>109315</epage><pages>109315-109315</pages><artnum>109315</artnum><issn>0009-2797</issn><eissn>1872-7786</eissn><abstract>Neutrophil infiltration, pro-inflammatory cytokines, and reactive oxygen species (ROS) production have been implicated in development and progression of ulcerative colitis (UC), an inflammatory bowel disease (IBD) characterized by ulcerating inflammation of the mucosal layer generally restricted to the colon. The side effects, safety and human intolerance are limitations of the currently approved treatments for UC. Hesperidin methyl chalcone (HMC) is a flavonoid used to treat chronic venous disease, which shows anti-inflammatory, analgesic, and antioxidant properties in pre-clinical studies, however, its effects on colitis have never been described. Therefore, we aimed to evaluate the protective effects of HMC in a mouse model of acetic acid-induced colitis. Treatment with HMC significantly reduced neutrophil infiltration, edema, colon shortening, macro and microscopic damages induced by intracolonic administration of acetic acid. The improvement of colitis after HMC treatment is related to the increase in colon antioxidant status, and the inhibition of pro-inflammatory cytokines TNF-α, IL-6, IL-1β, and IL-33 in the colon. We observed, moreover, that HMC inhibited NF-κB activation in the colon, which might explain the reduction of the cytokines we observed. Finally, these results demonstrate a novel applicability of HMC to increase antioxidant response and reduce inflammation during acetic acid-induced colitis suggesting it as a promising therapeutic approach for the treatment of ulcerative colitis.
•Methylation of hesperidin produces hesperidin methyl chalcone (HMC).•HMC inhibited neutrophil infiltration, edema and colon shortening in mouse colitis.•HMC also inhibited macroscopic and microscopic damages in colitis.•HMC reduced oxidative stress, cytokine production and NF-κB activation.•This is the first study demonstrating that HMC treats experimental ulcerative colitis.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>33171134</pmid><doi>10.1016/j.cbi.2020.109315</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Antioxidants - pharmacology Antioxidants - therapeutic use Chalcones - pharmacology Chalcones - therapeutic use Colitis, Ulcerative - complications Colitis, Ulcerative - drug therapy Colitis, Ulcerative - immunology Colitis, Ulcerative - metabolism Colon - drug effects Colon - pathology Cytokines - biosynthesis Disease Models, Animal Edema - complications Hesperidin - analogs & derivatives Hesperidin - pharmacology Hesperidin - therapeutic use Hesperidin methyl chalcone Inflammation Male Mice Neutrophil Infiltration - drug effects NF-kappa B - metabolism Oxidative stress Oxidative Stress - drug effects Ulcerative colitis |
title | Antioxidant and anti-inflammatory effects of hesperidin methyl chalcone in experimental ulcerative colitis |
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