Fig. 5: J2H-1702 controls macrophage polarization by inhibiting IL-1β. | Cell Death & Disease

Fig. 5: J2H-1702 controls macrophage polarization by inhibiting IL-1β.

From: Inhibition of 11β-hydroxysteroid dehydrogenase 1 alleviates pulmonary fibrosis through inhibition of endothelial-to-mesenchymal transition and M2 macrophage polarization by upregulating heme oxygenase-1

Fig. 5

A Expression of 11βHSD1 in monolayer (two-dimensional) cultures of various cell lines (A549, H460, H1299, HCAEC, HUVEC, WI38, THP-1) was detected by western blot. B, C HO-1 ELISA was performed with THP-1 cells. HO-1 expression was increased by treatment with 1 μM or 3 μM J2H-1702 (B) or by co-treatment with J2H-1702 and TGF-β1 (C). D THP-1 cell fractionation was performed, and expression of Nrf2 in the cytoplasmic and soluble nuclear extracts was detected. Lamin A/C was used as a nuclear marker, and GAPDH was used as a cytoplasmic marker. E, F Western blot was performed with THP-1 cells. Expression of the M2 macrophage marker Arginase 1 was increased by J2H-1702 treatment (E) or by co-treatment with J2H-1702 and bleomycin (F). G Treatment with 20 μM J2H-1702 resulted in elevated Arginase 1 mRNA expression in immune-activated MCLSs containing H460 cells. H The proteome profiler human cytokine array was used to analyze THP-1 cells treated with 1 μM J2H-1702. The spot size was decreased for IL-1β, and the spot expression was normalized against reference spots. I mRNA expression of IL-1β was analyzed in bleomycin-induced THP-1 cells and treated with J2H-1702. Data are shown as the mean ± standard deviation (n = 3). *P < 0.05 and **P < 0.01.

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