https://www.selleckchem.com/products/m344.html
In THP-1 cells, a human monocyte model, FA dose-dependently suppressed DNCB-elicited up-regulation of CD54 and CD86 at cell surface, secretion of pro-inflammatory cytokines IL-6 and TNF-α, and NFκB signaling activation.Conclusion Our findings demonstrated that FA could serve as a promising therapeutic agent in AD treatment.Pathological cardiac hypertrophy is a major risk factor for cardiovascular morbidity and mortality. Histone demethylases (KDMs) are emerging regulators of transcriptional reprograming in cancer, however, their potential
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