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651.
QIAO ZHOU JIAN LIU LING XIN YANYAN FANG LEI WAN DAN HUANG JIANTING WEN 《Biocell》2023,47(7):1623-1643
Objective: On the basis of data mining, systematic pharmacology, molecular docking, and experiment
validation, the oxidative-inflammatory molecular targets of Coicis Semen in the therapy of osteoarthritis (OA) were
explored. Methods: The association rule analysis was effectively applied to highlight the correlation between Coicis
Semen and oxidative inflammation indices. The random walk model was subsequently used to evaluate the clinical
efficacy of Coicis Semen. Network pharmacology was used to predict network targets. The binding affinity of the
active ingredient in Coicis Semen to the key target of OA was also successfully predicted. Results: Coicis Semen
showed a significant reduction in oxidative-inflammatory indicators of OA. A total of 108 promising targets were
predicted for the 24 bioactive compounds in Coicis Semen. Eight target genes were considered core target genes. The
enrichment analysis predicts that Coicis Semen may activate the interleukin (IL)-17, mitogen-activated protein kinase
(MAPK), and nuclear factor kappa B (NF-kappa B) signaling pathways. Molecular docking demonstrated that
stigmasterol, 2-monoolein, sitosterol, and sitosterol alpha1 had free binding energies to oxidative and inflammatory
targets (MAPK1, Estrogen Receptor 1 [ESR1], and Peroxisome Proliferator-Activated Receptor Alpha [PPARA]). Both
clinical trials and in vitro cell experiments revealed that Coicis Semen could increase ESR1 and PPAR-α levels while
decreasing MAPK1 levels. Conclusions: Coicis Semen has a remarkable anti-OA effect. Precisely, the major
components of Coicis Semen, including stigmasterol, sitosterol alpha1, sitosterol, and 2-monoolein, specifically inhibit
MAPK1, ESR1, and PPARA to reduce the inflammatory response and oxidative damage in OA. 相似文献
652.
QIAO ZHOU JIAN LIU LING XIN YANYAN FANG LEI WAN DAN HUANG JINCHEN GUO JIANTING WEN 《Biocell》2023,47(4):761-772
The pathophysiology of osteoarthritis (OA) is multifactorial, with the primary risk factors being obesity, age,
environmental variables, and genetic predisposition. The available evidence suggests that genetic diversity does not
adequately account for all clinical characteristics and heterogeneity of OA. Genetics has emerged as a nascent and
crucial area of research in OA. The epigenetic module presents a potential link between genetic and environmental
risk factors and the susceptibility and pathogenesis of OA. As a critical epigenetic alteration, DNA methylation has
been shown to have an important role in the etiology of OA and is a viable biomarker for predicting disease
progression and medication response, as shown in this research. This review aims to update knowledge in the field of
DNA methylation associated with OA to better identify the essential features of OA subtypes and pathological
conditions, hence accelerating individualized treatment and precision medicine. 相似文献