Icariin and icaritin ameliorated hippocampus neuroinflammation via inhibiting HMGB1-related pro-inflammatory signals in lipopolysaccharide-induced inflammation model in C57BL/6 J mice
Inflammation is a defensive response of the body and is at the center of many diseases' process like depression. High mobility group protein box 1 (HMGB1), has been proved to function as a pro-inflammatory cytokine. We aim to explore the role of HMGB1 played in the neuroinflammation here. In th...
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| Veröffentlicht in: | International immunopharmacology 2019-03, Vol.68, p.95-105 |
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| creator | Liu, Lumei Zhao, Zhengxiao Lu, Linwei Liu, Jiaqi Sun, Jing Wu, Xiao Dong, Jingcheng |
| description | Inflammation is a defensive response of the body and is at the center of many diseases' process like depression. High mobility group protein box 1 (HMGB1), has been proved to function as a pro-inflammatory cytokine. We aim to explore the role of HMGB1 played in the neuroinflammation here. In this study, we used LPS to induce an acute inflammatory response, and to measure the anti-neuroinflammation effect of icariin (ICA) and icaritin (ICT). We found that LPS could increase the expression of HMGB1 in serum and hippocampus, along with a high expression of HMGB1 in the cytoplasm and a high expression of RAGE, which could be rescued by ICA and ICT, and ethyl pyruvate (EP) pretreatment showed similar effects here. We speculated that the translocation of HMGB1 from the nucleus to the cytoplasm played an important role in neuroinflammatory process, and HMGB1-RAGE signal was involved in this process. Furthermore, we found that ICA and ICT treatment activated TLR4-XBP1s related NF-κB signal, which we thought was relevant with the neuroprotective effect of ICA and ICT. However, EP pretreatment suppressed TLR4-XBP1s- endoplasmic reticulum stress related NF-κB signal to anti-inflammatory response, which was almost absolutely opposite with ICA and ICT treatment. We speculated that it might be caused by the duration of inflammation. We supposed that ICA and ICT could ameliorate neuroinflammation in hippocampus via suppressing HMGB1-RAGE signaling and might show a neuroprotective effect via activating TLR4-XBP1s related NF-κB signal at the same time, making it possible to act as an anti-neuroinflammatory drugs.
•HMGB1-RAGE signaling and TLR4-XBP1s-NF-κB signaling were involved in neuroinflammation.•Icariin and icaritin could ameliorate neuroinflammation via suppressing HMGB1-RAGE signaling.•Icariin and icaritin might promote neuroregeneration via activating TLR4-NF-κB signaling. |
| doi_str_mv | 10.1016/j.intimp.2018.12.055 |
| format | Article |
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•HMGB1-RAGE signaling and TLR4-XBP1s-NF-κB signaling were involved in neuroinflammation.•Icariin and icaritin could ameliorate neuroinflammation via suppressing HMGB1-RAGE signaling.•Icariin and icaritin might promote neuroregeneration via activating TLR4-NF-κB signaling.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2018.12.055</identifier><identifier>PMID: 30616172</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Cytoplasm ; Defensive behavior ; Endoplasmic reticulum ; High mobility group proteins ; Hippocampus ; HMGB1 ; HMGB1 protein ; Icariin ; Icaritin ; Inflammation ; Inflammatory response ; Lipopolysaccharides ; Mental depression ; Neurogenesis ; Neuroinflammation ; Neuroprotection ; NF-κB protein ; Proteins ; Pyruvic acid ; Rodents ; Signal processing ; TLR4 protein ; Toll-like receptors ; Translocation</subject><ispartof>International immunopharmacology, 2019-03, Vol.68, p.95-105</ispartof><rights>2018</rights><rights>Copyright © 2018. Published by Elsevier B.V.</rights><rights>Copyright Elsevier BV Mar 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-4045b6f6e7d8adcd4085a91d110a94715a5d701ff11a036754daa1f14488a6273</citedby><cites>FETCH-LOGICAL-c390t-4045b6f6e7d8adcd4085a91d110a94715a5d701ff11a036754daa1f14488a6273</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2018.12.055$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30616172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Lumei</creatorcontrib><creatorcontrib>Zhao, Zhengxiao</creatorcontrib><creatorcontrib>Lu, Linwei</creatorcontrib><creatorcontrib>Liu, Jiaqi</creatorcontrib><creatorcontrib>Sun, Jing</creatorcontrib><creatorcontrib>Wu, Xiao</creatorcontrib><creatorcontrib>Dong, Jingcheng</creatorcontrib><title>Icariin and icaritin ameliorated hippocampus neuroinflammation via inhibiting HMGB1-related pro-inflammatory signals in lipopolysaccharide-induced inflammation model in C57BL/6 J mice</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>Inflammation is a defensive response of the body and is at the center of many diseases' process like depression. High mobility group protein box 1 (HMGB1), has been proved to function as a pro-inflammatory cytokine. We aim to explore the role of HMGB1 played in the neuroinflammation here. In this study, we used LPS to induce an acute inflammatory response, and to measure the anti-neuroinflammation effect of icariin (ICA) and icaritin (ICT). We found that LPS could increase the expression of HMGB1 in serum and hippocampus, along with a high expression of HMGB1 in the cytoplasm and a high expression of RAGE, which could be rescued by ICA and ICT, and ethyl pyruvate (EP) pretreatment showed similar effects here. We speculated that the translocation of HMGB1 from the nucleus to the cytoplasm played an important role in neuroinflammatory process, and HMGB1-RAGE signal was involved in this process. Furthermore, we found that ICA and ICT treatment activated TLR4-XBP1s related NF-κB signal, which we thought was relevant with the neuroprotective effect of ICA and ICT. However, EP pretreatment suppressed TLR4-XBP1s- endoplasmic reticulum stress related NF-κB signal to anti-inflammatory response, which was almost absolutely opposite with ICA and ICT treatment. We speculated that it might be caused by the duration of inflammation. We supposed that ICA and ICT could ameliorate neuroinflammation in hippocampus via suppressing HMGB1-RAGE signaling and might show a neuroprotective effect via activating TLR4-XBP1s related NF-κB signal at the same time, making it possible to act as an anti-neuroinflammatory drugs.
•HMGB1-RAGE signaling and TLR4-XBP1s-NF-κB signaling were involved in neuroinflammation.•Icariin and icaritin could ameliorate neuroinflammation via suppressing HMGB1-RAGE signaling.•Icariin and icaritin might promote neuroregeneration via activating TLR4-NF-κB signaling.</description><subject>Cytoplasm</subject><subject>Defensive behavior</subject><subject>Endoplasmic reticulum</subject><subject>High mobility group proteins</subject><subject>Hippocampus</subject><subject>HMGB1</subject><subject>HMGB1 protein</subject><subject>Icariin</subject><subject>Icaritin</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Lipopolysaccharides</subject><subject>Mental depression</subject><subject>Neurogenesis</subject><subject>Neuroinflammation</subject><subject>Neuroprotection</subject><subject>NF-κB protein</subject><subject>Proteins</subject><subject>Pyruvic acid</subject><subject>Rodents</subject><subject>Signal processing</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>Translocation</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp9kc9u1DAQxiMEoqXwBghZ4tJLtp7E_3JBoitoixZxgbPltZ3urJI42EmlvfFGnHkdngSHLZXgwMnj0e_7RjNfUbwEugIK4mK_wmHCflxVFNQKqhXl_FFxCkqqEiTlj3PNhSy5FM1J8SylPaW5z-BpcVJTAQJkdVr8uLEmIg7EDI7gUk_Lp_cdhmgm78gOxzFY049zIoOfY8Ch7UzfmwnDQO7QEBx2uF10t-T649UllNF3v6VjDOUDHeKBJLwdTJeygnQ4hjF0h2Ss3eWxzmfUzTbL_hrQB-e7RbDm8nJzIX5--_6B9Gj98-JJm738i_v3rPjy_t3n9XW5-XR1s367KW3d0KlklPGtaIWXThlnHaOKmwYcADUNk8ANd5JC2wIYWgvJmTMGWmBMKSMqWZ8V50ffvM3X2adJ95is7zoz-DAnXYHgtG4aoTL6-h90H-a4bJyppgamarUYsiNlY0gp-laPEXsTDxqoXqLVe32MVi_Raqh0jjbLXt2bz9veuwfRnywz8OYI-HyNO_RRJ4t-yBfF6O2kXcD_T_gFbSK63g</recordid><startdate>20190301</startdate><enddate>20190301</enddate><creator>Liu, Lumei</creator><creator>Zhao, Zhengxiao</creator><creator>Lu, Linwei</creator><creator>Liu, Jiaqi</creator><creator>Sun, Jing</creator><creator>Wu, Xiao</creator><creator>Dong, Jingcheng</creator><general>Elsevier B.V</general><general>Elsevier BV</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20190301</creationdate><title>Icariin and icaritin ameliorated hippocampus neuroinflammation via inhibiting HMGB1-related pro-inflammatory signals in lipopolysaccharide-induced inflammation model in C57BL/6 J mice</title><author>Liu, Lumei ; Zhao, Zhengxiao ; Lu, Linwei ; Liu, Jiaqi ; Sun, Jing ; Wu, Xiao ; Dong, Jingcheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-4045b6f6e7d8adcd4085a91d110a94715a5d701ff11a036754daa1f14488a6273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Cytoplasm</topic><topic>Defensive behavior</topic><topic>Endoplasmic reticulum</topic><topic>High mobility group proteins</topic><topic>Hippocampus</topic><topic>HMGB1</topic><topic>HMGB1 protein</topic><topic>Icariin</topic><topic>Icaritin</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Lipopolysaccharides</topic><topic>Mental depression</topic><topic>Neurogenesis</topic><topic>Neuroinflammation</topic><topic>Neuroprotection</topic><topic>NF-κB protein</topic><topic>Proteins</topic><topic>Pyruvic acid</topic><topic>Rodents</topic><topic>Signal processing</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Lumei</creatorcontrib><creatorcontrib>Zhao, Zhengxiao</creatorcontrib><creatorcontrib>Lu, Linwei</creatorcontrib><creatorcontrib>Liu, Jiaqi</creatorcontrib><creatorcontrib>Sun, Jing</creatorcontrib><creatorcontrib>Wu, Xiao</creatorcontrib><creatorcontrib>Dong, Jingcheng</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Lumei</au><au>Zhao, Zhengxiao</au><au>Lu, Linwei</au><au>Liu, Jiaqi</au><au>Sun, Jing</au><au>Wu, Xiao</au><au>Dong, Jingcheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Icariin and icaritin ameliorated hippocampus neuroinflammation via inhibiting HMGB1-related pro-inflammatory signals in lipopolysaccharide-induced inflammation model in C57BL/6 J mice</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2019-03-01</date><risdate>2019</risdate><volume>68</volume><spage>95</spage><epage>105</epage><pages>95-105</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>Inflammation is a defensive response of the body and is at the center of many diseases' process like depression. High mobility group protein box 1 (HMGB1), has been proved to function as a pro-inflammatory cytokine. We aim to explore the role of HMGB1 played in the neuroinflammation here. In this study, we used LPS to induce an acute inflammatory response, and to measure the anti-neuroinflammation effect of icariin (ICA) and icaritin (ICT). We found that LPS could increase the expression of HMGB1 in serum and hippocampus, along with a high expression of HMGB1 in the cytoplasm and a high expression of RAGE, which could be rescued by ICA and ICT, and ethyl pyruvate (EP) pretreatment showed similar effects here. We speculated that the translocation of HMGB1 from the nucleus to the cytoplasm played an important role in neuroinflammatory process, and HMGB1-RAGE signal was involved in this process. Furthermore, we found that ICA and ICT treatment activated TLR4-XBP1s related NF-κB signal, which we thought was relevant with the neuroprotective effect of ICA and ICT. However, EP pretreatment suppressed TLR4-XBP1s- endoplasmic reticulum stress related NF-κB signal to anti-inflammatory response, which was almost absolutely opposite with ICA and ICT treatment. We speculated that it might be caused by the duration of inflammation. We supposed that ICA and ICT could ameliorate neuroinflammation in hippocampus via suppressing HMGB1-RAGE signaling and might show a neuroprotective effect via activating TLR4-XBP1s related NF-κB signal at the same time, making it possible to act as an anti-neuroinflammatory drugs.
•HMGB1-RAGE signaling and TLR4-XBP1s-NF-κB signaling were involved in neuroinflammation.•Icariin and icaritin could ameliorate neuroinflammation via suppressing HMGB1-RAGE signaling.•Icariin and icaritin might promote neuroregeneration via activating TLR4-NF-κB signaling.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>30616172</pmid><doi>10.1016/j.intimp.2018.12.055</doi><tpages>11</tpages></addata></record> |
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| subjects | Cytoplasm Defensive behavior Endoplasmic reticulum High mobility group proteins Hippocampus HMGB1 HMGB1 protein Icariin Icaritin Inflammation Inflammatory response Lipopolysaccharides Mental depression Neurogenesis Neuroinflammation Neuroprotection NF-κB protein Proteins Pyruvic acid Rodents Signal processing TLR4 protein Toll-like receptors Translocation |
| title | Icariin and icaritin ameliorated hippocampus neuroinflammation via inhibiting HMGB1-related pro-inflammatory signals in lipopolysaccharide-induced inflammation model in C57BL/6 J mice |
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