Methane-Rich Saline Counteracts Cholestasis-Induced Liver Damage via Regulating the TLR4/NF-κB/NLRP3 Inflammasome Pathway
Cholestatic liver injury, due to obstruction of the biliary tract or genetic defects, is often accompanied by progressive inflammation and liver fibrosis. Methane-rich saline (MRS) has anti-inflammatory properties. However, whether MRS can provide protective effect in cholestatic liver injury is sti...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-13 |
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| creator | Zhang, Jingyao Liu, Chang Cui, Ruixia Tong, Yingmu Wang, Cong Feng, Yang Jia, Yifan Chen, Dongdong Li, Zeyu Qu, Kai |
| description | Cholestatic liver injury, due to obstruction of the biliary tract or genetic defects, is often accompanied by progressive inflammation and liver fibrosis. Methane-rich saline (MRS) has anti-inflammatory properties. However, whether MRS can provide protective effect in cholestatic liver injury is still unclear. In this study, Sprague-Dawley rats received bile duct ligation (BDL) to generate a cholestatic model followed by MRS treatment (10 mL/kg, ip treatment) every 12 h after the operation to explore the potential protective mechanism of MRS in cholestatic liver injury. We found that MRS effectively improved liver function, alleviated liver pathological damage, and localized infiltration of inflammatory cells. MRS treatment decreased the expression of hepatic fibrosis-associated proteins to alleviate liver fibrosis. Furthermore, MRS treatment suppressed the TLR4/NF-κB pathway and further reduced the levels of proinflammatory factors. Downregulation of NF-κB subsequently reduced the NLRP3 expression to inhibit pyroptosis. Our data indicated that methane treatment prevented cholestatic liver injury via anti-inflammatory properties that involved the TLR4/NF-κB/NLRP3 signaling pathway. |
| doi_str_mv | 10.1155/2019/6565283 |
| format | Article |
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Methane-rich saline (MRS) has anti-inflammatory properties. However, whether MRS can provide protective effect in cholestatic liver injury is still unclear. In this study, Sprague-Dawley rats received bile duct ligation (BDL) to generate a cholestatic model followed by MRS treatment (10 mL/kg, ip treatment) every 12 h after the operation to explore the potential protective mechanism of MRS in cholestatic liver injury. We found that MRS effectively improved liver function, alleviated liver pathological damage, and localized infiltration of inflammatory cells. MRS treatment decreased the expression of hepatic fibrosis-associated proteins to alleviate liver fibrosis. Furthermore, MRS treatment suppressed the TLR4/NF-κB pathway and further reduced the levels of proinflammatory factors. Downregulation of NF-κB subsequently reduced the NLRP3 expression to inhibit pyroptosis. Our data indicated that methane treatment prevented cholestatic liver injury via anti-inflammatory properties that involved the TLR4/NF-κB/NLRP3 signaling pathway.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2019/6565283</identifier><identifier>PMID: 31827690</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Bile ; Bile Ducts ; Biotechnology ; Cholestasis - complications ; Cytokines ; Gallbladder diseases ; Gene Expression Regulation - drug effects ; Hepatitis ; Immunoglobulins ; Inflammasomes - drug effects ; Inflammation ; Inflammation - etiology ; Inflammation - pathology ; Inflammation - prevention & control ; Ischemia ; Ligation ; Liver diseases ; Liver Diseases - etiology ; Liver Diseases - pathology ; Liver Diseases - prevention & control ; Male ; Medical research ; Methane - pharmacology ; NF-kappa B - genetics ; NF-kappa B - metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Proteins ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Sodium Chloride - pharmacology ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - metabolism ; Tumor necrosis factor-TNF</subject><ispartof>Oxidative medicine and cellular longevity, 2019, Vol.2019 (2019), p.1-13</ispartof><rights>Copyright © 2019 Zeyu Li et al.</rights><rights>Copyright © 2019 Zeyu Li et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Zeyu Li et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-cf258ae5101fb2d1c2f3e36547322b3fbfafd4a1164beb844d45dc499b77e5843</citedby><cites>FETCH-LOGICAL-c471t-cf258ae5101fb2d1c2f3e36547322b3fbfafd4a1164beb844d45dc499b77e5843</cites><orcidid>0000-0002-2700-7531 ; 0000-0002-1138-3727 ; 0000-0002-8227-9396 ; 0000-0002-7318-1004</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885841/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885841/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31827690$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Victor, Victor M.</contributor><creatorcontrib>Zhang, Jingyao</creatorcontrib><creatorcontrib>Liu, Chang</creatorcontrib><creatorcontrib>Cui, Ruixia</creatorcontrib><creatorcontrib>Tong, Yingmu</creatorcontrib><creatorcontrib>Wang, Cong</creatorcontrib><creatorcontrib>Feng, Yang</creatorcontrib><creatorcontrib>Jia, Yifan</creatorcontrib><creatorcontrib>Chen, Dongdong</creatorcontrib><creatorcontrib>Li, Zeyu</creatorcontrib><creatorcontrib>Qu, Kai</creatorcontrib><title>Methane-Rich Saline Counteracts Cholestasis-Induced Liver Damage via Regulating the TLR4/NF-κB/NLRP3 Inflammasome Pathway</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Cholestatic liver injury, due to obstruction of the biliary tract or genetic defects, is often accompanied by progressive inflammation and liver fibrosis. Methane-rich saline (MRS) has anti-inflammatory properties. However, whether MRS can provide protective effect in cholestatic liver injury is still unclear. In this study, Sprague-Dawley rats received bile duct ligation (BDL) to generate a cholestatic model followed by MRS treatment (10 mL/kg, ip treatment) every 12 h after the operation to explore the potential protective mechanism of MRS in cholestatic liver injury. We found that MRS effectively improved liver function, alleviated liver pathological damage, and localized infiltration of inflammatory cells. MRS treatment decreased the expression of hepatic fibrosis-associated proteins to alleviate liver fibrosis. Furthermore, MRS treatment suppressed the TLR4/NF-κB pathway and further reduced the levels of proinflammatory factors. Downregulation of NF-κB subsequently reduced the NLRP3 expression to inhibit pyroptosis. Our data indicated that methane treatment prevented cholestatic liver injury via anti-inflammatory properties that involved the TLR4/NF-κB/NLRP3 signaling pathway.</description><subject>Animals</subject><subject>Bile</subject><subject>Bile Ducts</subject><subject>Biotechnology</subject><subject>Cholestasis - complications</subject><subject>Cytokines</subject><subject>Gallbladder diseases</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hepatitis</subject><subject>Immunoglobulins</subject><subject>Inflammasomes - drug effects</subject><subject>Inflammation</subject><subject>Inflammation - etiology</subject><subject>Inflammation - pathology</subject><subject>Inflammation - prevention & control</subject><subject>Ischemia</subject><subject>Ligation</subject><subject>Liver diseases</subject><subject>Liver Diseases - etiology</subject><subject>Liver Diseases - pathology</subject><subject>Liver Diseases - prevention & control</subject><subject>Male</subject><subject>Medical research</subject><subject>Methane - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Jingyao</au><au>Liu, Chang</au><au>Cui, Ruixia</au><au>Tong, Yingmu</au><au>Wang, Cong</au><au>Feng, Yang</au><au>Jia, Yifan</au><au>Chen, Dongdong</au><au>Li, Zeyu</au><au>Qu, Kai</au><au>Victor, Victor M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methane-Rich Saline Counteracts Cholestasis-Induced Liver Damage via Regulating the TLR4/NF-κB/NLRP3 Inflammasome Pathway</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2019</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>13</epage><pages>1-13</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Cholestatic liver injury, due to obstruction of the biliary tract or genetic defects, is often accompanied by progressive inflammation and liver fibrosis. Methane-rich saline (MRS) has anti-inflammatory properties. However, whether MRS can provide protective effect in cholestatic liver injury is still unclear. In this study, Sprague-Dawley rats received bile duct ligation (BDL) to generate a cholestatic model followed by MRS treatment (10 mL/kg, ip treatment) every 12 h after the operation to explore the potential protective mechanism of MRS in cholestatic liver injury. We found that MRS effectively improved liver function, alleviated liver pathological damage, and localized infiltration of inflammatory cells. MRS treatment decreased the expression of hepatic fibrosis-associated proteins to alleviate liver fibrosis. Furthermore, MRS treatment suppressed the TLR4/NF-κB pathway and further reduced the levels of proinflammatory factors. Downregulation of NF-κB subsequently reduced the NLRP3 expression to inhibit pyroptosis. Our data indicated that methane treatment prevented cholestatic liver injury via anti-inflammatory properties that involved the TLR4/NF-κB/NLRP3 signaling pathway.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>31827690</pmid><doi>10.1155/2019/6565283</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-2700-7531</orcidid><orcidid>https://orcid.org/0000-0002-1138-3727</orcidid><orcidid>https://orcid.org/0000-0002-8227-9396</orcidid><orcidid>https://orcid.org/0000-0002-7318-1004</orcidid><oa>free_for_read</oa></addata></record> |
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| source | PubMed (Medline); Wiley-Blackwell Open Access Collection; MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library; PubMed Central Open Access |
| subjects | Animals Bile Bile Ducts Biotechnology Cholestasis - complications Cytokines Gallbladder diseases Gene Expression Regulation - drug effects Hepatitis Immunoglobulins Inflammasomes - drug effects Inflammation Inflammation - etiology Inflammation - pathology Inflammation - prevention & control Ischemia Ligation Liver diseases Liver Diseases - etiology Liver Diseases - pathology Liver Diseases - prevention & control Male Medical research Methane - pharmacology NF-kappa B - genetics NF-kappa B - metabolism NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Proteins Rats Rats, Sprague-Dawley Signal Transduction Sodium Chloride - pharmacology Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism Tumor necrosis factor-TNF |
| title | Methane-Rich Saline Counteracts Cholestasis-Induced Liver Damage via Regulating the TLR4/NF-κB/NLRP3 Inflammasome Pathway |
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