Silibinin Mitigates Vanadium-induced Lung Injury via the TLR4/MAPK/NF-κB Pathway in Mice
Silibinin, has been investigated for its potential benefits and mechanisms in addressing vanadium pentoxide (V2O5)-induced pulmonary inflammation. This study explored the anti-inflammatory activity of silibinin and elucidate the mechanisms by which it operates in a mouse model of vanadium-induced lu...
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Veröffentlicht in: | In vivo (Athens) 2024-09, Vol.38 (5), p.2179-2189 |
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creator | Im, Hobin Kim, Eungyung Kwon, Hong Ju Kim, Hyeonjin Ko, Jiwon Sung, Yonghun Kim, Sung-Hyun Lee, Eun Jung Kwon, Woo-Sung Ryoo, Zae Young Yi, Junkoo Park, Si Jun Kim, Myoung Ok |
description | Silibinin, has been investigated for its potential benefits and mechanisms in addressing vanadium pentoxide (V2O5)-induced pulmonary inflammation. This study explored the anti-inflammatory activity of silibinin and elucidate the mechanisms by which it operates in a mouse model of vanadium-induced lung injury.
Eight-week-old male BALB/c mice were exposed to V2O5 to induce lung injury. Mice were pretreated with silibinin at doses of 50 mg/kg and 100 mg/kg. Histological analyses were performed to assess cell viability and infiltration of inflammatory cells. The expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and activation of the MAPK and NF-[Formula: see text]B signaling pathways, as well as the NLRP3 inflammasome, were evaluated using real-time PCR, western blot analysis, and immunohistochemistry. Whole blood analysis was conducted to measure white blood cell counts.
Silibinin treatment significantly improved cell viability, reduced inflammatory cell infiltration, and decreased the expression of pro-inflammatory cytokines in V2O5-induced lung injury. It also notably suppressed the activation of the MAPK and NF-[Formula: see text]B signaling pathways, along with a marked reduction in NLRP3 inflammasome expression levels in lung tissues. Additionally, silibinin-treated groups exhibited a significant decrease in white blood cell counts, including neutrophils, lymphocytes, and eosinophils.
These findings underscore the potent anti-inflammatory effects of silibinin in mice with V2O5-induced lung inflammation, highlighting its therapeutic potential. The study not only confirms the efficacy of silibinin in mitigating inflammatory responses but also provides a foundational understanding of its role in modulating key inflammatory pathways, paving the way for future therapeutic strategies against pulmonary inflammation induced by environmental pollutants. |
doi_str_mv | 10.21873/invivo.13681 |
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Eight-week-old male BALB/c mice were exposed to V2O5 to induce lung injury. Mice were pretreated with silibinin at doses of 50 mg/kg and 100 mg/kg. Histological analyses were performed to assess cell viability and infiltration of inflammatory cells. The expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and activation of the MAPK and NF-[Formula: see text]B signaling pathways, as well as the NLRP3 inflammasome, were evaluated using real-time PCR, western blot analysis, and immunohistochemistry. Whole blood analysis was conducted to measure white blood cell counts.
Silibinin treatment significantly improved cell viability, reduced inflammatory cell infiltration, and decreased the expression of pro-inflammatory cytokines in V2O5-induced lung injury. It also notably suppressed the activation of the MAPK and NF-[Formula: see text]B signaling pathways, along with a marked reduction in NLRP3 inflammasome expression levels in lung tissues. Additionally, silibinin-treated groups exhibited a significant decrease in white blood cell counts, including neutrophils, lymphocytes, and eosinophils.
These findings underscore the potent anti-inflammatory effects of silibinin in mice with V2O5-induced lung inflammation, highlighting its therapeutic potential. The study not only confirms the efficacy of silibinin in mitigating inflammatory responses but also provides a foundational understanding of its role in modulating key inflammatory pathways, paving the way for future therapeutic strategies against pulmonary inflammation induced by environmental pollutants.</description><identifier>ISSN: 0258-851X</identifier><identifier>ISSN: 1791-7549</identifier><identifier>EISSN: 1791-7549</identifier><identifier>DOI: 10.21873/invivo.13681</identifier><identifier>PMID: 39187362</identifier><language>eng</language><publisher>Greece</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Cytokines - metabolism ; Disease Models, Animal ; Inflammation Mediators - metabolism ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Lung Injury - chemically induced ; Lung Injury - drug therapy ; Lung Injury - etiology ; Lung Injury - metabolism ; Lung Injury - pathology ; Male ; Mice ; Mice, Inbred BALB C ; NF-kappa B - metabolism ; Signal Transduction - drug effects ; Silybin - pharmacology ; Silymarin - pharmacology ; Toll-Like Receptor 4 - metabolism ; Vanadium - pharmacology</subject><ispartof>In vivo (Athens), 2024-09, Vol.38 (5), p.2179-2189</ispartof><rights>Copyright © 2024, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39187362$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Im, Hobin</creatorcontrib><creatorcontrib>Kim, Eungyung</creatorcontrib><creatorcontrib>Kwon, Hong Ju</creatorcontrib><creatorcontrib>Kim, Hyeonjin</creatorcontrib><creatorcontrib>Ko, Jiwon</creatorcontrib><creatorcontrib>Sung, Yonghun</creatorcontrib><creatorcontrib>Kim, Sung-Hyun</creatorcontrib><creatorcontrib>Lee, Eun Jung</creatorcontrib><creatorcontrib>Kwon, Woo-Sung</creatorcontrib><creatorcontrib>Ryoo, Zae Young</creatorcontrib><creatorcontrib>Yi, Junkoo</creatorcontrib><creatorcontrib>Park, Si Jun</creatorcontrib><creatorcontrib>Kim, Myoung Ok</creatorcontrib><title>Silibinin Mitigates Vanadium-induced Lung Injury via the TLR4/MAPK/NF-κB Pathway in Mice</title><title>In vivo (Athens)</title><addtitle>In Vivo</addtitle><description>Silibinin, has been investigated for its potential benefits and mechanisms in addressing vanadium pentoxide (V2O5)-induced pulmonary inflammation. This study explored the anti-inflammatory activity of silibinin and elucidate the mechanisms by which it operates in a mouse model of vanadium-induced lung injury.
Eight-week-old male BALB/c mice were exposed to V2O5 to induce lung injury. Mice were pretreated with silibinin at doses of 50 mg/kg and 100 mg/kg. Histological analyses were performed to assess cell viability and infiltration of inflammatory cells. The expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and activation of the MAPK and NF-[Formula: see text]B signaling pathways, as well as the NLRP3 inflammasome, were evaluated using real-time PCR, western blot analysis, and immunohistochemistry. Whole blood analysis was conducted to measure white blood cell counts.
Silibinin treatment significantly improved cell viability, reduced inflammatory cell infiltration, and decreased the expression of pro-inflammatory cytokines in V2O5-induced lung injury. It also notably suppressed the activation of the MAPK and NF-[Formula: see text]B signaling pathways, along with a marked reduction in NLRP3 inflammasome expression levels in lung tissues. Additionally, silibinin-treated groups exhibited a significant decrease in white blood cell counts, including neutrophils, lymphocytes, and eosinophils.
These findings underscore the potent anti-inflammatory effects of silibinin in mice with V2O5-induced lung inflammation, highlighting its therapeutic potential. The study not only confirms the efficacy of silibinin in mitigating inflammatory responses but also provides a foundational understanding of its role in modulating key inflammatory pathways, paving the way for future therapeutic strategies against pulmonary inflammation induced by environmental pollutants.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Inflammation Mediators - metabolism</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung Injury - chemically induced</subject><subject>Lung Injury - drug therapy</subject><subject>Lung Injury - etiology</subject><subject>Lung Injury - metabolism</subject><subject>Lung Injury - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>NF-kappa B - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Silybin - pharmacology</subject><subject>Silymarin - pharmacology</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Vanadium - pharmacology</subject><issn>0258-851X</issn><issn>1791-7549</issn><issn>1791-7549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1PwjAAhhujEUSPXk2PXgbt2vXjiESUOJQoMXpauq6DEtbhumH4a_4If5MI6Om9PO9zeAC4xKgbYsFJz7q1XZddTJjAR6CNucQBj6g8Bm0URiIQEX5rgTPvFwgxjlB4ClpE_l5Z2AbvL3ZpU-usg2Nb25mqjYevyqnMNkVgXdZok8G4cTM4coum2sC1VbCeGziNn2lv3J889B6HwffXDZyoev6pNnCn0uYcnORq6c3FYTtgOrydDu6D-OluNOjHgZY0DESoMyIMJiJnSFEkKKUoJ4gJriXjTOpMhjTUKpWUIxkhIxWjVFGccpJiSjrgeq9dVeVHY3ydFNZrs1wqZ8rGJwRJTiXmlG3RYI_qqvS-Mnmyqmyhqk2CUbKLmexjJruYW_7qoG7SwmT_9F898gNSp28J</recordid><startdate>202409</startdate><enddate>202409</enddate><creator>Im, Hobin</creator><creator>Kim, Eungyung</creator><creator>Kwon, Hong Ju</creator><creator>Kim, Hyeonjin</creator><creator>Ko, Jiwon</creator><creator>Sung, Yonghun</creator><creator>Kim, Sung-Hyun</creator><creator>Lee, Eun Jung</creator><creator>Kwon, Woo-Sung</creator><creator>Ryoo, Zae Young</creator><creator>Yi, Junkoo</creator><creator>Park, Si Jun</creator><creator>Kim, Myoung Ok</creator><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>202409</creationdate><title>Silibinin Mitigates Vanadium-induced Lung Injury via the TLR4/MAPK/NF-κB Pathway in Mice</title><author>Im, Hobin ; Kim, Eungyung ; Kwon, Hong Ju ; Kim, Hyeonjin ; Ko, Jiwon ; Sung, Yonghun ; Kim, Sung-Hyun ; Lee, Eun Jung ; Kwon, Woo-Sung ; Ryoo, Zae Young ; Yi, Junkoo ; Park, Si Jun ; Kim, Myoung Ok</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c942-82cd38e138f60a4084440f30687c96769cd9242cab9470950e9a644a41b73b143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Inflammation Mediators - metabolism</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lung Injury - chemically induced</topic><topic>Lung Injury - drug therapy</topic><topic>Lung Injury - etiology</topic><topic>Lung Injury - metabolism</topic><topic>Lung Injury - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>NF-kappa B - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Silybin - pharmacology</topic><topic>Silymarin - pharmacology</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Vanadium - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Im, Hobin</creatorcontrib><creatorcontrib>Kim, Eungyung</creatorcontrib><creatorcontrib>Kwon, Hong Ju</creatorcontrib><creatorcontrib>Kim, Hyeonjin</creatorcontrib><creatorcontrib>Ko, Jiwon</creatorcontrib><creatorcontrib>Sung, Yonghun</creatorcontrib><creatorcontrib>Kim, Sung-Hyun</creatorcontrib><creatorcontrib>Lee, Eun Jung</creatorcontrib><creatorcontrib>Kwon, Woo-Sung</creatorcontrib><creatorcontrib>Ryoo, Zae Young</creatorcontrib><creatorcontrib>Yi, Junkoo</creatorcontrib><creatorcontrib>Park, Si Jun</creatorcontrib><creatorcontrib>Kim, Myoung Ok</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>In vivo (Athens)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Im, Hobin</au><au>Kim, Eungyung</au><au>Kwon, Hong Ju</au><au>Kim, Hyeonjin</au><au>Ko, Jiwon</au><au>Sung, Yonghun</au><au>Kim, Sung-Hyun</au><au>Lee, Eun Jung</au><au>Kwon, Woo-Sung</au><au>Ryoo, Zae Young</au><au>Yi, Junkoo</au><au>Park, Si Jun</au><au>Kim, Myoung Ok</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silibinin Mitigates Vanadium-induced Lung Injury via the TLR4/MAPK/NF-κB Pathway in Mice</atitle><jtitle>In vivo (Athens)</jtitle><addtitle>In Vivo</addtitle><date>2024-09</date><risdate>2024</risdate><volume>38</volume><issue>5</issue><spage>2179</spage><epage>2189</epage><pages>2179-2189</pages><issn>0258-851X</issn><issn>1791-7549</issn><eissn>1791-7549</eissn><abstract>Silibinin, has been investigated for its potential benefits and mechanisms in addressing vanadium pentoxide (V2O5)-induced pulmonary inflammation. This study explored the anti-inflammatory activity of silibinin and elucidate the mechanisms by which it operates in a mouse model of vanadium-induced lung injury.
Eight-week-old male BALB/c mice were exposed to V2O5 to induce lung injury. Mice were pretreated with silibinin at doses of 50 mg/kg and 100 mg/kg. Histological analyses were performed to assess cell viability and infiltration of inflammatory cells. The expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and activation of the MAPK and NF-[Formula: see text]B signaling pathways, as well as the NLRP3 inflammasome, were evaluated using real-time PCR, western blot analysis, and immunohistochemistry. Whole blood analysis was conducted to measure white blood cell counts.
Silibinin treatment significantly improved cell viability, reduced inflammatory cell infiltration, and decreased the expression of pro-inflammatory cytokines in V2O5-induced lung injury. It also notably suppressed the activation of the MAPK and NF-[Formula: see text]B signaling pathways, along with a marked reduction in NLRP3 inflammasome expression levels in lung tissues. Additionally, silibinin-treated groups exhibited a significant decrease in white blood cell counts, including neutrophils, lymphocytes, and eosinophils.
These findings underscore the potent anti-inflammatory effects of silibinin in mice with V2O5-induced lung inflammation, highlighting its therapeutic potential. The study not only confirms the efficacy of silibinin in mitigating inflammatory responses but also provides a foundational understanding of its role in modulating key inflammatory pathways, paving the way for future therapeutic strategies against pulmonary inflammation induced by environmental pollutants.</abstract><cop>Greece</cop><pmid>39187362</pmid><doi>10.21873/invivo.13681</doi><tpages>11</tpages></addata></record> |
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subjects | Animals Anti-Inflammatory Agents - pharmacology Cytokines - metabolism Disease Models, Animal Inflammation Mediators - metabolism Lung - drug effects Lung - metabolism Lung - pathology Lung Injury - chemically induced Lung Injury - drug therapy Lung Injury - etiology Lung Injury - metabolism Lung Injury - pathology Male Mice Mice, Inbred BALB C NF-kappa B - metabolism Signal Transduction - drug effects Silybin - pharmacology Silymarin - pharmacology Toll-Like Receptor 4 - metabolism Vanadium - pharmacology |
title | Silibinin Mitigates Vanadium-induced Lung Injury via the TLR4/MAPK/NF-κB Pathway in Mice |
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