<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ji J</submitter><funding>National Natural Science Foundation of China</funding><pagination>242</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7247226</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Cardiac fibroblasts, regarded as the immunomodulatory hub of the heart, have been thought to play an important role during sepsis-induced cardiomyopathy (SIC). However, the detailed molecular mechanism and targeted therapies for SIC are still lacking. Therefore, we sought to investigate the likely protective effects of rolipram, an anti-inflammatory drug, on lipopolysaccharide (LPS)-stimulated inflammatory responses in cardiac fibroblasts and on cardiac dysfunction in endotoxic mice.&lt;h4>Method&lt;/h4>Cardiac fibroblasts were isolated and stimulated with 1 μg/ml LPS for 6 h, and 10 μmol/l rolipram was administered for 1 h before LPS stimulation. mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in fibroblasts and their protein co</pubmed_abstract><journal>BMC cardiovascular disorders</journal><pubmed_title>Protective effects of rolipram on endotoxic cardiac dysfunction via inhibition of the inflammatory response in cardiac fibroblasts.</pubmed_title><pmcid>PMC7247226</pmcid><funding_grant_id>81571940; 81741125</funding_grant_id><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Hong X</pubmed_authors><pubmed_authors>Gao J</pubmed_authors><pubmed_authors>Ji J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Protective effects of rolipram on endotoxic cardiac dysfunction via inhibition of the inflammatory response in cardiac fibroblasts.</name><description>&lt;h4>Background&lt;/h4>Cardiac fibroblasts, regarded as the immunomodulatory hub of the heart, have been thought to play an important role during sepsis-induced cardiomyopathy (SIC). However, the detailed molecular mechanism and targeted therapies for SIC are still lacking. Therefore, we sought to investigate the likely protective effects of rolipram, an anti-inflammatory drug, on lipopolysaccharide (LPS)-stimulated inflammatory responses in cardiac fibroblasts and on cardiac dysfunction in endotoxic mice.&lt;h4>Method&lt;/h4>Cardiac fibroblasts were isolated and stimulated with 1 μg/ml LPS for 6 h, and 10 μmol/l rolipram was administered for 1 h before LPS stimulation. mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in fibroblasts and their protein co</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 May</publication><modification>2025-04-25T21:37:44.656Z</modification><creation>2020-06-05T07:04:53Z</creation></dates><accession>S-EPMC7247226</accession><cross_references><pubmed>32448150</pubmed><doi>10.1186/s12872-020-01529-7</doi></cross_references></HashMap>