ArticleInflammopharmacology2026
Screening of active constituents in camellia oil against atopic dermatitis via molecular docking and experimental validation: elucidation of the underlying molecular mechanism.
Article in Inflammopharmacology, 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
objectiveAtopic dermatitis (AD) is a chronic inflammatory skin disease. The JAK/STAT and PDE4/cAMP pathways are pivotal in driving its inflammation. This study aimed to discover natural JAK1 and PDE4 inhibitors from camellia oil to alleviate AD.
methodsUtilizing the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), we employed a target-based molecular docking approach against key inflammatory targets (JAK1, PDE4B, PDE4D) of AD to screen the compounds in camellia oil. This virtual screening was followed by in vitro enzymatic assays to validate their inhibitory effects. Based on these findings, we employed a DNCB-induced AD mouse model to compare the therapeutic efficacy of (1% and 4%) ( +)-catechin hydrate and (4% and 6%) epicatechin against 1.5% ruxolitinib cream.
resultsAlthough molecular docking screening predicted seven compounds with potential high binding affinity for PDE4B and PDE4D, respectively, subsequent in vitro enzymatic inhibition assays demonstrated that all of these compounds exhibited low inhibitory rates against the enzymes. In comparison, (+)-catechin hydrate and epicatechin not only exhibited excellent binding affinity with JAK1 but also achieved high inhibition rates. Their IC
conclusionIn camellia oil, (+)-catechin hydrate and epicatechin are the primary active constituents for the treatment of AD, suggesting that their anti-AD effects were possibly mediated through the suppression of the JAK1-driven inflammatory signaling pathway. This study not only provides a novel utilization strategy for camellia oil, but also offers new insights for the treatment of AD.
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