Effect of PKG on the secretion of inflammatory cytokines in THP-1 macrophage-derived foam cells

Objective To investigate the effect of PKG on the secretion of IL-6, IL-10, and TNF-α inTHP-1 macrophage-derived foam cells. Methods THP-1 monocytes were induced to construct macrophages by treating with 160 nmol / L TPA. Then the macrophages were further treated with 50 mg / L ox-LDL to become foam cells. Four groups were set in this study, including the macrophage group, the foam cell group, the group of foam cell treated with PKG agonist 8-Br-cGMP, and the group of foam cell treated with PKG inhibitor KT-5823. The morphology of THP-1 cells, macrophages and foam cells were observed under microscope. The cellular lipid accumulation was detected by oil red ostaining. The secretion of IL-6, IL-10, and TNF-α into the supernatant was detected by ELISA assay. Results The foam cell was obtained after macrophage incubated with ox-LDL for 48hours. The secretion of IL-6 and TNF-α increased significantly from the foam cells than that from the macrophages(P 0.05). After the THP-1 monocyte-derived macrophages were incubated with 8-Br-cGMP, the secretion of IL-6in the supernatant decreased significantly(P 0.05) and IL-10 level in the supernatant increased significantly(P 0.05). After the macrophages were incubated with KT-5823, the secretion of IL-10 decreased significantly(P 0.05), but the secretion of IL-6 was not significantly changed(P 0.05). After incubation with 8-Br-cGMP,the secretion of IL-6 and TNF-α from the macrophage-derived foam cells decreased significantly(P 0.05), but IL-10 increased significantly(P 0.05). After the foam cells were treated with KT-5823, the secretion of IL-6 and TNF-α were also decreased significantly(P 0.05), with no significant change of IL-10 secretion(P 0.05).Conclusions PKG may enhance the expression of anti-inflammatory cytokine IL-10, and inhibit the expression of inflammatory cytokine IL-6 and TNF-α, contributing to prevent the development of inflammation. PKG might have a potential anti-atherosclerosis effect.