ArticleScientific reports2026
Mechanism elucidation of Polygonatum sibiricum-Prepared Cervus elaphus velvet antler in intervening non-alcoholic fatty liver disease based on network analysis combined with proteomics.
Article in Scientific reports, 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
To establish the standardized processing technology of velvet antler stir-fried with Polygonatum sibiricum juice, elucidate the core mechanism underlying the enhanced anti-non-alcoholic fatty liver disease (NAFLD) efficacy of the processed product, and identify the key bioactive components. Taking protein content as the screening index, this study optimized the processing parameters of Polygonatum sibiricum-Prepared Cervus elaphus Velvet Antler (PC-PR) using single-factor experiments combined with response surface methodology (RSM). The in vivo pharmacodynamic efficacy was validated in a high-fat diet-induced NAFLD rat model. Multi-omics technologies were integrated to screen for core differential proteins enriched after processing. The in vitro activity of the target component was verified in an oleic acid-induced inflammatory model of HepG2 cells, and Western blot (WB) analysis was employed to decipher its molecular regulatory mechanism. A standardized processing technology for PC-PR was successfully established, which induced specific alterations in the compositional profile of velvet antler. The processed product significantly improved blood glucose, body weight, liver function, and lipid metabolism indicators in NAFLD model rats, with superior efficacy compared to non-optimally processed velvet antler. Multi-omics screening and in vitro experiments confirmed that Q28237 is a core bioactive component specifically enriched after processing, exhibiting potent lipid-lowering and anti-inflammatory activities. Mechanistic studies revealed that Q28237 alleviates the pathological progression of NAFLD by constructing a "component-pathway-phenotype" regulatory network, which involves inhibiting the overactivation of epidermal growth factor receptor (EGFR), promoting the activation of the phosphatidylinositol 3-kinase-protein kinase B (PI3K-AKT) pathway, and activating estrogen receptor1 (ESR1) to exert synergisticanti-inflammatory effects.
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