Silymarin prevents NLRP3 inflammasome activation and protects against intracerebral hemorrhage
Inflammatory response mediates secondary injury during intracerebral hemorrhage (ICH). In the present study, we determined oxidative stress and involvement of NLRP3 in ICH injury and analyzed whether silymarin might offer protective effect against ICH injury. Post 24h after ICH injury there was incr...
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| Veröffentlicht in: | Biomedicine & pharmacotherapy 2017-09, Vol.93, p.308-315 |
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| creator | Yuan, Raorao Fan, Hengyi Cheng, Shiqi Gao, WeiWei Xu, Xin Lv, Shigang Ye, Minhua Wu, Miaojing Zhu, Xingen Zhang, Yan |
| description | Inflammatory response mediates secondary injury during intracerebral hemorrhage (ICH). In the present study, we determined oxidative stress and involvement of NLRP3 in ICH injury and analyzed whether silymarin might offer protective effect against ICH injury. Post 24h after ICH injury there was increased oxidative stress markers (reactive oxygen species (ROS) and lipid peroxides) compared to sham group. Silymarin (200mg/kg) treatment 30 mins post ICH injury prevented increase in oxidative stress markers and up-regulated antioxidant status. Further, there was significant increase in nuclear levels of NF-κB-p65 and pro-inflammatory cytokine expressions post ICH injury. NLRP3 inflammasome activation and downstream targets such as caspase-1 and IL-1β expressions were significantly up regulated in ICH injury. Silymarin treatment significantly down regulated the inflammatory responses by suppressing NF-κB-p65 levels and inflammasome-mediated caspase-1/IL-1β expressions. Further, treatment with silymarin post ICH injury increased Nrf-2/HO-1 and thereby improved overall cytoprotection. These findings together show that silymarin acts as neuroprotective compound by preventing inflammatory activation and up regulating Nrf-2/HO-1 signaling post ICH injury. |
| doi_str_mv | 10.1016/j.biopha.2017.06.018 |
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In the present study, we determined oxidative stress and involvement of NLRP3 in ICH injury and analyzed whether silymarin might offer protective effect against ICH injury. Post 24h after ICH injury there was increased oxidative stress markers (reactive oxygen species (ROS) and lipid peroxides) compared to sham group. Silymarin (200mg/kg) treatment 30 mins post ICH injury prevented increase in oxidative stress markers and up-regulated antioxidant status. Further, there was significant increase in nuclear levels of NF-κB-p65 and pro-inflammatory cytokine expressions post ICH injury. NLRP3 inflammasome activation and downstream targets such as caspase-1 and IL-1β expressions were significantly up regulated in ICH injury. Silymarin treatment significantly down regulated the inflammatory responses by suppressing NF-κB-p65 levels and inflammasome-mediated caspase-1/IL-1β expressions. Further, treatment with silymarin post ICH injury increased Nrf-2/HO-1 and thereby improved overall cytoprotection. These findings together show that silymarin acts as neuroprotective compound by preventing inflammatory activation and up regulating Nrf-2/HO-1 signaling post ICH injury.</description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2017.06.018</identifier><identifier>PMID: 28651232</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Animals ; Antioxidants - metabolism ; Caspase 1 - metabolism ; Cerebral Hemorrhage - drug therapy ; Cerebral Hemorrhage - metabolism ; Disease Models, Animal ; Down-Regulation - drug effects ; ICH ; Inflammasome ; Inflammasomes - metabolism ; Interleukin-1beta - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B - metabolism ; NF-κB-P65 ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 ; Nrf-2 ; Oxidative Stress - drug effects ; Protective Agents - pharmacology ; Reactive Oxygen Species - metabolism ; Signal Transduction - drug effects ; Silymarin ; Silymarin - pharmacology ; Up-Regulation - drug effects</subject><ispartof>Biomedicine & pharmacotherapy, 2017-09, Vol.93, p.308-315</ispartof><rights>2017 Elsevier Masson SAS</rights><rights>Copyright © 2017 Elsevier Masson SAS. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-a71e9cd4509badd54bca724277454f239448bf32fb19aadf0700ae56396a38873</citedby><cites>FETCH-LOGICAL-c362t-a71e9cd4509badd54bca724277454f239448bf32fb19aadf0700ae56396a38873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0753332217315846$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28651232$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yuan, Raorao</creatorcontrib><creatorcontrib>Fan, Hengyi</creatorcontrib><creatorcontrib>Cheng, Shiqi</creatorcontrib><creatorcontrib>Gao, WeiWei</creatorcontrib><creatorcontrib>Xu, Xin</creatorcontrib><creatorcontrib>Lv, Shigang</creatorcontrib><creatorcontrib>Ye, Minhua</creatorcontrib><creatorcontrib>Wu, Miaojing</creatorcontrib><creatorcontrib>Zhu, Xingen</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><title>Silymarin prevents NLRP3 inflammasome activation and protects against intracerebral hemorrhage</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description>Inflammatory response mediates secondary injury during intracerebral hemorrhage (ICH). In the present study, we determined oxidative stress and involvement of NLRP3 in ICH injury and analyzed whether silymarin might offer protective effect against ICH injury. Post 24h after ICH injury there was increased oxidative stress markers (reactive oxygen species (ROS) and lipid peroxides) compared to sham group. Silymarin (200mg/kg) treatment 30 mins post ICH injury prevented increase in oxidative stress markers and up-regulated antioxidant status. Further, there was significant increase in nuclear levels of NF-κB-p65 and pro-inflammatory cytokine expressions post ICH injury. NLRP3 inflammasome activation and downstream targets such as caspase-1 and IL-1β expressions were significantly up regulated in ICH injury. Silymarin treatment significantly down regulated the inflammatory responses by suppressing NF-κB-p65 levels and inflammasome-mediated caspase-1/IL-1β expressions. Further, treatment with silymarin post ICH injury increased Nrf-2/HO-1 and thereby improved overall cytoprotection. These findings together show that silymarin acts as neuroprotective compound by preventing inflammatory activation and up regulating Nrf-2/HO-1 signaling post ICH injury.</description><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>Caspase 1 - metabolism</subject><subject>Cerebral Hemorrhage - drug therapy</subject><subject>Cerebral Hemorrhage - metabolism</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation - drug effects</subject><subject>ICH</subject><subject>Inflammasome</subject><subject>Inflammasomes - metabolism</subject><subject>Interleukin-1beta - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB-P65</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3</subject><subject>Nrf-2</subject><subject>Oxidative Stress - drug effects</subject><subject>Protective Agents - pharmacology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Silymarin</subject><subject>Silymarin - pharmacology</subject><subject>Up-Regulation - drug effects</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P3DAQhq2KqrtA_0FV5cglYfyROL4gVYgWpFVbQbnWmjiTXa_ysbWzK_Hva7TAkdNcnnfemYexLxwKDry63BaNn3YbLARwXUBVAK8_sCU3JeQVgD5hS9ClzKUUYsFOY9wCQFnJ-hNbiLoquZBiyf4--P5pwODHbBfoQOMcs5-r-98y82PX4zBgnAbK0M3-gLOfxgzHNqHTTC6huEY_xjnBc0BHgZqAfbahYQphg2s6Zx877CN9fpln7PH7zZ_r23z168fd9bdV7mQl5hw1J-NaVYJpsG1L1TjUQgmtVak6IY1SddNJ0TXcILYdaACk9IypUNa1lmfs4rg3XfZvT3G2g4-O-h5HmvbRcsOVqI0qTULVEXVhijFQZ3fBJwNPloN9Nmu39mjWPpu1UNlkNsW-vjTsm4Hat9CrygRcHQFKfx48BRudp9FR60NyZdvJv9_wH9HQjPU</recordid><startdate>201709</startdate><enddate>201709</enddate><creator>Yuan, Raorao</creator><creator>Fan, Hengyi</creator><creator>Cheng, Shiqi</creator><creator>Gao, WeiWei</creator><creator>Xu, Xin</creator><creator>Lv, Shigang</creator><creator>Ye, Minhua</creator><creator>Wu, Miaojing</creator><creator>Zhu, Xingen</creator><creator>Zhang, Yan</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></search><sort><creationdate>201709</creationdate><title>Silymarin prevents NLRP3 inflammasome activation and protects against intracerebral hemorrhage</title><author>Yuan, Raorao ; Fan, Hengyi ; Cheng, Shiqi ; Gao, WeiWei ; Xu, Xin ; Lv, Shigang ; Ye, Minhua ; Wu, Miaojing ; Zhu, Xingen ; Zhang, Yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-a71e9cd4509badd54bca724277454f239448bf32fb19aadf0700ae56396a38873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>Caspase 1 - metabolism</topic><topic>Cerebral Hemorrhage - drug therapy</topic><topic>Cerebral Hemorrhage - metabolism</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation - drug effects</topic><topic>ICH</topic><topic>Inflammasome</topic><topic>Inflammasomes - metabolism</topic><topic>Interleukin-1beta - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB-P65</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3</topic><topic>Nrf-2</topic><topic>Oxidative Stress - drug effects</topic><topic>Protective Agents - pharmacology</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Silymarin</topic><topic>Silymarin - pharmacology</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yuan, Raorao</creatorcontrib><creatorcontrib>Fan, Hengyi</creatorcontrib><creatorcontrib>Cheng, Shiqi</creatorcontrib><creatorcontrib>Gao, WeiWei</creatorcontrib><creatorcontrib>Xu, Xin</creatorcontrib><creatorcontrib>Lv, Shigang</creatorcontrib><creatorcontrib>Ye, Minhua</creatorcontrib><creatorcontrib>Wu, Miaojing</creatorcontrib><creatorcontrib>Zhu, Xingen</creatorcontrib><creatorcontrib>Zhang, Yan</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>Yuan, Raorao</au><au>Fan, Hengyi</au><au>Cheng, Shiqi</au><au>Gao, WeiWei</au><au>Xu, Xin</au><au>Lv, Shigang</au><au>Ye, Minhua</au><au>Wu, Miaojing</au><au>Zhu, Xingen</au><au>Zhang, Yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silymarin prevents NLRP3 inflammasome activation and protects against intracerebral hemorrhage</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2017-09</date><risdate>2017</risdate><volume>93</volume><spage>308</spage><epage>315</epage><pages>308-315</pages><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract>Inflammatory response mediates secondary injury during intracerebral hemorrhage (ICH). In the present study, we determined oxidative stress and involvement of NLRP3 in ICH injury and analyzed whether silymarin might offer protective effect against ICH injury. Post 24h after ICH injury there was increased oxidative stress markers (reactive oxygen species (ROS) and lipid peroxides) compared to sham group. Silymarin (200mg/kg) treatment 30 mins post ICH injury prevented increase in oxidative stress markers and up-regulated antioxidant status. Further, there was significant increase in nuclear levels of NF-κB-p65 and pro-inflammatory cytokine expressions post ICH injury. NLRP3 inflammasome activation and downstream targets such as caspase-1 and IL-1β expressions were significantly up regulated in ICH injury. Silymarin treatment significantly down regulated the inflammatory responses by suppressing NF-κB-p65 levels and inflammasome-mediated caspase-1/IL-1β expressions. Further, treatment with silymarin post ICH injury increased Nrf-2/HO-1 and thereby improved overall cytoprotection. These findings together show that silymarin acts as neuroprotective compound by preventing inflammatory activation and up regulating Nrf-2/HO-1 signaling post ICH injury.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>28651232</pmid><doi>10.1016/j.biopha.2017.06.018</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Antioxidants - metabolism Caspase 1 - metabolism Cerebral Hemorrhage - drug therapy Cerebral Hemorrhage - metabolism Disease Models, Animal Down-Regulation - drug effects ICH Inflammasome Inflammasomes - metabolism Interleukin-1beta - metabolism Male Mice Mice, Inbred C57BL NF-kappa B - metabolism NF-κB-P65 NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 Nrf-2 Oxidative Stress - drug effects Protective Agents - pharmacology Reactive Oxygen Species - metabolism Signal Transduction - drug effects Silymarin Silymarin - pharmacology Up-Regulation - drug effects |
| title | Silymarin prevents NLRP3 inflammasome activation and protects against intracerebral hemorrhage |
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