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Casticin prevents DSS induced ulcerative colitis in mice through inhibitions of NF‐κB pathway and ROS signaling
Casticin, a compound purified from the Chinese herb Viticis Fructus, has been proven effective in preventing tumor progression in previous studies. Ulcerative colitis (UC) is a common inflammatory bowel disease that affects millions of people worldwide, but no effective and safe drugs are available....
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| Published in: | Phytotherapy research 2018-09, Vol.32 (9), p.1770-1783 |
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| creator | Ma, Jiamei Yin, Ganghui Lu, Zibin Xie, Pei Zhou, Hongling Liu, Junshan Yu, Linzhong |
| description | Casticin, a compound purified from the Chinese herb Viticis Fructus, has been proven effective in preventing tumor progression in previous studies. Ulcerative colitis (UC) is a common inflammatory bowel disease that affects millions of people worldwide, but no effective and safe drugs are available. In this study, we aimed to study how did casticin affect UC by evaluating its effects on dextran sulfate sodium (DSS)‐induced colitis in mice. Our data suggested that casticin attenuated body weight loss, colon length shortening, and pathological damage in the colon of DSS‐treated mice. Casticin decreased reactive oxygen species level and chemocytokines (IL‐1β, IL‐6, TNF‐α) productions in colon tissue. The decreased reactive oxygen species level and suppressed proinflammatory cytokines productions were also confirmed in casticin‐treated LPS‐stimulated RAW264.7 cells and hydrogen peroxide‐treated CACO‐2 cells in vitro. Mechanistically, casticin treatment prevented the profound activation of AKT signaling caused by DSS administration. And casticin inhibited the productions of proinflammatory chemocytokines through downregulating AKT/NF‐κB pathway in macrophages. Meanwhile, data revealed that casticin increased expressions of endogenous antioxidants peroxiredoxin 3 and MnSOD were through activation in FOXO3α signaling by downregulating AKT signaling in colon epithelium cells. Our findings demonstrated that casticin alleviated DSS‐induced UC by increasing the antioxidant enzyme peroxiredoxin 3 and MnSOD expressions, and decreasing the production of proinflammatory chemocytokines through inhibition of AKT signaling. |
| doi_str_mv | 10.1002/ptr.6108 |
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Ulcerative colitis (UC) is a common inflammatory bowel disease that affects millions of people worldwide, but no effective and safe drugs are available. In this study, we aimed to study how did casticin affect UC by evaluating its effects on dextran sulfate sodium (DSS)‐induced colitis in mice. Our data suggested that casticin attenuated body weight loss, colon length shortening, and pathological damage in the colon of DSS‐treated mice. Casticin decreased reactive oxygen species level and chemocytokines (IL‐1β, IL‐6, TNF‐α) productions in colon tissue. The decreased reactive oxygen species level and suppressed proinflammatory cytokines productions were also confirmed in casticin‐treated LPS‐stimulated RAW264.7 cells and hydrogen peroxide‐treated CACO‐2 cells in vitro. Mechanistically, casticin treatment prevented the profound activation of AKT signaling caused by DSS administration. And casticin inhibited the productions of proinflammatory chemocytokines through downregulating AKT/NF‐κB pathway in macrophages. Meanwhile, data revealed that casticin increased expressions of endogenous antioxidants peroxiredoxin 3 and MnSOD were through activation in FOXO3α signaling by downregulating AKT signaling in colon epithelium cells. Our findings demonstrated that casticin alleviated DSS‐induced UC by increasing the antioxidant enzyme peroxiredoxin 3 and MnSOD expressions, and decreasing the production of proinflammatory chemocytokines through inhibition of AKT signaling.</description><identifier>ISSN: 0951-418X</identifier><identifier>EISSN: 1099-1573</identifier><identifier>DOI: 10.1002/ptr.6108</identifier><identifier>PMID: 29876982</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Activation ; AKT protein ; Animals ; Antioxidants ; Body weight ; Body weight loss ; Caco-2 Cells ; Colitis, Ulcerative - chemically induced ; Colitis, Ulcerative - drug therapy ; Colon ; Cytokines ; Dextran ; Dextran Sulfate ; Disease Models, Animal ; Epithelium ; Flavonoids - pharmacology ; Humans ; Hydrogen peroxide ; IL-1β ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Interleukin-1beta - metabolism ; Interleukin-6 - metabolism ; Intestine ; Lipopolysaccharides ; Macrophages ; Macrophages - drug effects ; Male ; Mice ; NF-kappa B - metabolism ; Peroxiredoxin ; Peroxiredoxin III - metabolism ; RAW 264.7 Cells ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Sodium ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - metabolism ; Ulcerative colitis ; Weight loss</subject><ispartof>Phytotherapy research, 2018-09, Vol.32 (9), p.1770-1783</ispartof><rights>Copyright © 2018 John Wiley & Sons, Ltd.</rights><rights>2018 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2648-9ee25f9665de323cc72cb0dafe5c6f1a5f84a1136d59e6814e679dce2c59030d3</citedby><cites>FETCH-LOGICAL-c2648-9ee25f9665de323cc72cb0dafe5c6f1a5f84a1136d59e6814e679dce2c59030d3</cites><orcidid>0000-0003-3164-7045</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,783,787,27936,27937</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29876982$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Jiamei</creatorcontrib><creatorcontrib>Yin, Ganghui</creatorcontrib><creatorcontrib>Lu, Zibin</creatorcontrib><creatorcontrib>Xie, Pei</creatorcontrib><creatorcontrib>Zhou, Hongling</creatorcontrib><creatorcontrib>Liu, Junshan</creatorcontrib><creatorcontrib>Yu, Linzhong</creatorcontrib><title>Casticin prevents DSS induced ulcerative colitis in mice through inhibitions of NF‐κB pathway and ROS signaling</title><title>Phytotherapy research</title><addtitle>Phytother Res</addtitle><description>Casticin, a compound purified from the Chinese herb Viticis Fructus, has been proven effective in preventing tumor progression in previous studies. Ulcerative colitis (UC) is a common inflammatory bowel disease that affects millions of people worldwide, but no effective and safe drugs are available. In this study, we aimed to study how did casticin affect UC by evaluating its effects on dextran sulfate sodium (DSS)‐induced colitis in mice. Our data suggested that casticin attenuated body weight loss, colon length shortening, and pathological damage in the colon of DSS‐treated mice. Casticin decreased reactive oxygen species level and chemocytokines (IL‐1β, IL‐6, TNF‐α) productions in colon tissue. The decreased reactive oxygen species level and suppressed proinflammatory cytokines productions were also confirmed in casticin‐treated LPS‐stimulated RAW264.7 cells and hydrogen peroxide‐treated CACO‐2 cells in vitro. Mechanistically, casticin treatment prevented the profound activation of AKT signaling caused by DSS administration. And casticin inhibited the productions of proinflammatory chemocytokines through downregulating AKT/NF‐κB pathway in macrophages. Meanwhile, data revealed that casticin increased expressions of endogenous antioxidants peroxiredoxin 3 and MnSOD were through activation in FOXO3α signaling by downregulating AKT signaling in colon epithelium cells. Our findings demonstrated that casticin alleviated DSS‐induced UC by increasing the antioxidant enzyme peroxiredoxin 3 and MnSOD expressions, and decreasing the production of proinflammatory chemocytokines through inhibition of AKT signaling.</description><subject>Activation</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Body weight</subject><subject>Body weight loss</subject><subject>Caco-2 Cells</subject><subject>Colitis, Ulcerative - chemically induced</subject><subject>Colitis, Ulcerative - drug therapy</subject><subject>Colon</subject><subject>Cytokines</subject><subject>Dextran</subject><subject>Dextran Sulfate</subject><subject>Disease Models, Animal</subject><subject>Epithelium</subject><subject>Flavonoids - pharmacology</subject><subject>Humans</subject><subject>Hydrogen peroxide</subject><subject>IL-1β</subject><subject>Inflammatory bowel disease</subject><subject>Inflammatory bowel diseases</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-6 - metabolism</subject><subject>Intestine</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Male</subject><subject>Mice</subject><subject>NF-kappa B - metabolism</subject><subject>Peroxiredoxin</subject><subject>Peroxiredoxin III - metabolism</subject><subject>RAW 264.7 Cells</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Sodium</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Ulcerative colitis</subject><subject>Weight loss</subject><issn>0951-418X</issn><issn>1099-1573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kd1KwzAUx4MoOj_AJ5CAN95Uk7RJm0udTgVR2RS8K1lyumV0bU3ajd35CD6PD-FD-CR2foLg1eHw__HjcP4I7VJySAlhR1XtDgUlyQrqUCJlQHkcrqIOkZwGEU0eNtCm9xNCiGQkWkcbTCaxkAnrINdVvrbaFrhyMIOi9vh0MMC2MI0Gg5tcg1O1nQHWZW5r69sIT60GXI9d2YzG7T62wzYpC4_LDF_33p6eX19OcKXq8VwtsCoM7t8MsLejQuW2GG2jtUzlHna-5ha6753ddS-Cq5vzy-7xVaCZiJJAAjCeSSG4gZCFWsdMD4lRGXAtMqp4lkSK0lAYLkEkNAIRS6OBaS5JSEy4hQ4-vZUrHxvwdTq1XkOeqwLKxqeMcCo4FyJs0f0_6KRsXHvukpIylkkoxa9Qu9J7B1laOTtVbpFSki57SNse0mUPLbr3JWyGUzA_4PfjWyD4BOY2h8W_ovT2rv8hfAfgIpOX</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Ma, Jiamei</creator><creator>Yin, Ganghui</creator><creator>Lu, Zibin</creator><creator>Xie, Pei</creator><creator>Zhou, Hongling</creator><creator>Liu, Junshan</creator><creator>Yu, Linzhong</creator><general>Wiley Subscription Services, Inc</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>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3164-7045</orcidid></search><sort><creationdate>201809</creationdate><title>Casticin prevents DSS induced ulcerative colitis in mice through inhibitions of NF‐κB pathway and ROS signaling</title><author>Ma, Jiamei ; Yin, Ganghui ; Lu, Zibin ; Xie, Pei ; Zhou, Hongling ; Liu, Junshan ; Yu, Linzhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2648-9ee25f9665de323cc72cb0dafe5c6f1a5f84a1136d59e6814e679dce2c59030d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activation</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Body weight</topic><topic>Body weight loss</topic><topic>Caco-2 Cells</topic><topic>Colitis, Ulcerative - chemically induced</topic><topic>Colitis, Ulcerative - drug therapy</topic><topic>Colon</topic><topic>Cytokines</topic><topic>Dextran</topic><topic>Dextran Sulfate</topic><topic>Disease Models, Animal</topic><topic>Epithelium</topic><topic>Flavonoids - pharmacology</topic><topic>Humans</topic><topic>Hydrogen peroxide</topic><topic>IL-1β</topic><topic>Inflammatory bowel disease</topic><topic>Inflammatory bowel diseases</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukin-6 - metabolism</topic><topic>Intestine</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Male</topic><topic>Mice</topic><topic>NF-kappa B - metabolism</topic><topic>Peroxiredoxin</topic><topic>Peroxiredoxin III - metabolism</topic><topic>RAW 264.7 Cells</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Sodium</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Ulcerative colitis</topic><topic>Weight loss</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Jiamei</creatorcontrib><creatorcontrib>Yin, Ganghui</creatorcontrib><creatorcontrib>Lu, Zibin</creatorcontrib><creatorcontrib>Xie, Pei</creatorcontrib><creatorcontrib>Zhou, Hongling</creatorcontrib><creatorcontrib>Liu, Junshan</creatorcontrib><creatorcontrib>Yu, Linzhong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Phytotherapy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Jiamei</au><au>Yin, Ganghui</au><au>Lu, Zibin</au><au>Xie, Pei</au><au>Zhou, Hongling</au><au>Liu, Junshan</au><au>Yu, Linzhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Casticin prevents DSS induced ulcerative colitis in mice through inhibitions of NF‐κB pathway and ROS signaling</atitle><jtitle>Phytotherapy research</jtitle><addtitle>Phytother Res</addtitle><date>2018-09</date><risdate>2018</risdate><volume>32</volume><issue>9</issue><spage>1770</spage><epage>1783</epage><pages>1770-1783</pages><issn>0951-418X</issn><eissn>1099-1573</eissn><abstract>Casticin, a compound purified from the Chinese herb Viticis Fructus, has been proven effective in preventing tumor progression in previous studies. Ulcerative colitis (UC) is a common inflammatory bowel disease that affects millions of people worldwide, but no effective and safe drugs are available. In this study, we aimed to study how did casticin affect UC by evaluating its effects on dextran sulfate sodium (DSS)‐induced colitis in mice. Our data suggested that casticin attenuated body weight loss, colon length shortening, and pathological damage in the colon of DSS‐treated mice. Casticin decreased reactive oxygen species level and chemocytokines (IL‐1β, IL‐6, TNF‐α) productions in colon tissue. The decreased reactive oxygen species level and suppressed proinflammatory cytokines productions were also confirmed in casticin‐treated LPS‐stimulated RAW264.7 cells and hydrogen peroxide‐treated CACO‐2 cells in vitro. Mechanistically, casticin treatment prevented the profound activation of AKT signaling caused by DSS administration. And casticin inhibited the productions of proinflammatory chemocytokines through downregulating AKT/NF‐κB pathway in macrophages. Meanwhile, data revealed that casticin increased expressions of endogenous antioxidants peroxiredoxin 3 and MnSOD were through activation in FOXO3α signaling by downregulating AKT signaling in colon epithelium cells. Our findings demonstrated that casticin alleviated DSS‐induced UC by increasing the antioxidant enzyme peroxiredoxin 3 and MnSOD expressions, and decreasing the production of proinflammatory chemocytokines through inhibition of AKT signaling.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29876982</pmid><doi>10.1002/ptr.6108</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-3164-7045</orcidid></addata></record> |
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| subjects | Activation AKT protein Animals Antioxidants Body weight Body weight loss Caco-2 Cells Colitis, Ulcerative - chemically induced Colitis, Ulcerative - drug therapy Colon Cytokines Dextran Dextran Sulfate Disease Models, Animal Epithelium Flavonoids - pharmacology Humans Hydrogen peroxide IL-1β Inflammatory bowel disease Inflammatory bowel diseases Interleukin-1beta - metabolism Interleukin-6 - metabolism Intestine Lipopolysaccharides Macrophages Macrophages - drug effects Male Mice NF-kappa B - metabolism Peroxiredoxin Peroxiredoxin III - metabolism RAW 264.7 Cells Reactive oxygen species Reactive Oxygen Species - metabolism Signal transduction Signal Transduction - drug effects Signaling Sodium Superoxide dismutase Superoxide Dismutase - metabolism Tumor necrosis factor Tumor Necrosis Factor-alpha - metabolism Ulcerative colitis Weight loss |
| title | Casticin prevents DSS induced ulcerative colitis in mice through inhibitions of NF‐κB pathway and ROS signaling |
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