ArticleApplied biochemistry and biotechnology2026
Solanum mauritianum Scop. Leaf Extract Attenuates ROS-Mediated Inflammation and Prevents IL-6 Promoter Demethylation in Activated Monocytes.
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Solanum mauritianum Scop. (SM) is a medicinal plant with ethnopharmacological relevance, noted for its diverse secondary metabolites. Despite its traditional use in inflammatory conditions, its mechanistic anti-inflammatory potential remains unexplored. This study investigates the molecular effects of SM leaf ethyl acetate extract (SMLE) on key inflammatory signalling pathways. Quantitative, qualitative and GC-MS mediated identification of phytoconstituents in SMLE was carried out. Preliminary screening for SMLE was carried out using DPPH, nitric oxide scavenging and protein denaturation assays. In vitro anti-inflammatory effect of SMLE was evaluated in PMA-activated THP-1 cells. FACS, RT-PCR, and ELISA were performed to measure intracellular ROS and proinflammatory cytokine expression (IL-6, IL-1β, TNF-α), respectively. Molecular docking of quercetin, a key SMLE compound, was studied. A change in DNA promoter methylation of IL-6 was performed using RFLP. Phenolics, alkaloids, and terpenoids were identified in SMLE, and GC-MS analysis revealed 24 compounds. A flavonoid, quercetin, was isolated and characterised from the extract. SMLE was biocompatible with both THP-1 and human PBMNCs. In PMA-activated THP-1 cells, SMLE reduced intracellular ROS by 83% compared to H₂O₂ controls and significantly (P < 0.001) downregulated IL-6 (2.3-fold ± 0.05), IL-1β (1.2-fold ± 0.05), and TNF-α (1.2-fold ± 0.08) expression at transcript and protein levels. Docking showed strong binding of quercetin to NOX2 (–8.72 kcal/mol). SMLE also maintained CpG methylation status at the IL-6 promoter region. Biocompatible SMLE downregulates inflammation in activated monocytes, potentially by binding to NOX2 and preventing ROS-mediated activation of the IL-6 gene promoter. Its strong in vitro anti-inflammatory efficacy, combined with low cytotoxicity, highlights SMLE as a promising candidate for anti-inflammatory therapeutics. By preserving CpG methylation at the IL-6 promoter, SMLE may offer an epigenetic means of limiting IL-6-driven chronic inflammation, which is clinically relevant in conditions such as atherosclerosis, arthritis, and other inflammatory disorders.
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