<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu QH</submitter><funding>The National Science and Technology Major Project for "Significant New Drugs Creation"</funding><funding>Xinjiang Production and Construction Corps Guiding Science and Technology Plan</funding><funding>Youth Innovative Talent Cultivation Projects of Shihezi University</funding><funding>the National Natural Science Foundation of China</funding><pagination>1875</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10856478</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(3)</volume><pubmed_abstract>Acute lung injury (ALI) is a serious inflammatory disease with high morbidity and mortality. Rosavin is an anti-inflammatory and antioxidant phenylpropanoid and glucoside, which is isolated from Rhodiola rosea L. However, its potential molecular mechanisms and whether it has protective effects against lipopolysaccharide (LPS)-induced ALI remain to be elucidated. To assess the in vitro anti-inflammatory effects and anti-lung injury activity of rosavin, RAW264.7 and A549 cells were stimulated using 1 μg/mL LPS. Rosavin attenuated LPS-induced activation of the TLR-4/NF-κB signaling pathway in RAW264.7 cells and inhibited LPS-induced release of inflammatory factors in A549 cells. A mouse model of acute lung injury was constructed by intraperitoneal injection of 5 mg/kg LPS to observe the therapeutic effect of rosavin. Transcriptomics analysis and Western blot assays were utilized to verify the molecular mechanism, rosavin (20, 40, and 80 mg/kg) dose-dependently ameliorated histopathological alterations, reduced the levels of inflammatory factors, and inhibited the TLR-4/NF-κB/MAPK signaling pathway and apoptosis activation. Rosavin is a promising therapeutic candidate for acute lung injury by inhibiting the TLR-4/NF-κB/MAPK pathway.</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Rosavin Alleviates LPS-Induced Acute Lung Injure by Modulating the TLR-4/NF-κB/MAPK Singnaling Pathways.</pubmed_title><pmcid>PMC10856478</pmcid><funding_grant_id>2022ZD008</funding_grant_id><funding_grant_id>No. ZX09735-005</funding_grant_id><funding_grant_id>No. 82004061</funding_grant_id><funding_grant_id>CXPY202220</funding_grant_id><pubmed_authors>Liu QH</pubmed_authors><pubmed_authors>Feng SS</pubmed_authors><pubmed_authors>Zhang K</pubmed_authors><pubmed_authors>Li SY</pubmed_authors><pubmed_authors>Zhang LJ</pubmed_authors><pubmed_authors>Wang JH</pubmed_authors><pubmed_authors>Wang HY</pubmed_authors></additional><is_claimable>false</is_claimable><name>Rosavin Alleviates LPS-Induced Acute Lung Injure by Modulating the TLR-4/NF-κB/MAPK Singnaling Pathways.</name><description>Acute lung injury (ALI) is a serious inflammatory disease with high morbidity and mortality. Rosavin is an anti-inflammatory and antioxidant phenylpropanoid and glucoside, which is isolated from Rhodiola rosea L. However, its potential molecular mechanisms and whether it has protective effects against lipopolysaccharide (LPS)-induced ALI remain to be elucidated. To assess the in vitro anti-inflammatory effects and anti-lung injury activity of rosavin, RAW264.7 and A549 cells were stimulated using 1 μg/mL LPS. Rosavin attenuated LPS-induced activation of the TLR-4/NF-κB signaling pathway in RAW264.7 cells and inhibited LPS-induced release of inflammatory factors in A549 cells. A mouse model of acute lung injury was constructed by intraperitoneal injection of 5 mg/kg LPS to observe the therapeutic effect of rosavin. Transcriptomics analysis and Western blot assays were utilized to verify the molecular mechanism, rosavin (20, 40, and 80 mg/kg) dose-dependently ameliorated histopathological alterations, reduced the levels of inflammatory factors, and inhibited the TLR-4/NF-κB/MAPK signaling pathway and apoptosis activation. Rosavin is a promising therapeutic candidate for acute lung injury by inhibiting the TLR-4/NF-κB/MAPK pathway.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Feb</publication><modification>2025-04-05T14:51:32.801Z</modification><creation>2025-04-05T14:51:32.801Z</creation></dates><accession>S-EPMC10856478</accession><cross_references><pubmed>38339153</pubmed><doi>10.3390/ijms25031875</doi></cross_references></HashMap>