<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11(5)</volume><submitter>Reddy Sankaran K</submitter><pubmed_abstract>&lt;i>Pterocarpus santalinus&lt;/i> has huge demand owing to its commercial and medicinal value. However, there are limited research studies on its therapeutic activity against obesity and obesity-induced inflammation and underlying mechanism of action. Therefore, in the present study, chloroform bioactive fraction of &lt;i>P. santalinus&lt;/i> (CFP) was isolated and evaluated for its activity against adipogenesis and adipogenesis-induced inflammation in 3T3-L1 cell culture model. LC-MS/MS analysis of CFP was performed to identify the compounds present. CFP-treated 3T3-L1 cells (50, 100 and 200 μg/ml) have significantly (&lt;i>p&lt;/i> &lt; 0.01 or &lt; 0.05) enhanced glycerol release and adiponectin level, but reduced lipid accumulation and leptin, and MTT assay demonstrated CFP was non-toxic till a dose of 300 µg/ml at 24 and 48 h. A considerable reduction in tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels was witnessed in lipopolysaccharide (LPS)-induced 3T3-L1 cells with CFP treatment in dose-dependent manner. Gene expression studies demonstrated down-regulation of mRNA expression of peroxisome proliferator-activated receptor-γ (PPAR-γ), sterol regulatory element-binding protein-1c (SREBP-1c), leptin, TNF-α and IL-6 but up-regulation of adiponectin and uncoupling protein-1 (UCP-1) and the same trend was observed in protein expression also. In conclusion, it is suggested that CFP could be beneficial to treat obesity and associated inflammation.</pubmed_abstract><journal>3 Biotech</journal><pagination>233</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8065073</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A bioactive fraction of &lt;i>Pterocarpus santalinus&lt;/i> inhibits adipogenesis and inflammation in 3T3-L1 cells via modulation of PPAR-γ/SREBP-1c and TNF-α/IL-6.</pubmed_title><pmcid>PMC8065073</pmcid><pubmed_authors>Reddy Sankaran K</pubmed_authors><pubmed_authors>Chippada AR</pubmed_authors><pubmed_authors>Ganjayi MS</pubmed_authors><pubmed_authors>Oruganti L</pubmed_authors><pubmed_authors>Meriga B</pubmed_authors></additional><is_claimable>false</is_claimable><name>A bioactive fraction of &lt;i>Pterocarpus santalinus&lt;/i> inhibits adipogenesis and inflammation in 3T3-L1 cells via modulation of PPAR-γ/SREBP-1c and TNF-α/IL-6.</name><description>&lt;i>Pterocarpus santalinus&lt;/i> has huge demand owing to its commercial and medicinal value. However, there are limited research studies on its therapeutic activity against obesity and obesity-induced inflammation and underlying mechanism of action. Therefore, in the present study, chloroform bioactive fraction of &lt;i>P. santalinus&lt;/i> (CFP) was isolated and evaluated for its activity against adipogenesis and adipogenesis-induced inflammation in 3T3-L1 cell culture model. LC-MS/MS analysis of CFP was performed to identify the compounds present. CFP-treated 3T3-L1 cells (50, 100 and 200 μg/ml) have significantly (&lt;i>p&lt;/i> &lt; 0.01 or &lt; 0.05) enhanced glycerol release and adiponectin level, but reduced lipid accumulation and leptin, and MTT assay demonstrated CFP was non-toxic till a dose of 300 µg/ml at 24 and 48 h. A considerable reduction in tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels was witnessed in lipopolysaccharide (LPS)-induced 3T3-L1 cells with CFP treatment in dose-dependent manner. Gene expression studies demonstrated down-regulation of mRNA expression of peroxisome proliferator-activated receptor-γ (PPAR-γ), sterol regulatory element-binding protein-1c (SREBP-1c), leptin, TNF-α and IL-6 but up-regulation of adiponectin and uncoupling protein-1 (UCP-1) and the same trend was observed in protein expression also. In conclusion, it is suggested that CFP could be beneficial to treat obesity and associated inflammation.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 May</publication><modification>2024-11-09T07:56:13.222Z</modification><creation>2024-11-09T07:56:13.222Z</creation></dates><accession>S-EPMC8065073</accession><cross_references><pubmed>33968577</pubmed><doi>10.1007/s13205-021-02771-2</doi></cross_references></HashMap>