Study On Rapid Nongenmoic Effects Of Glucocorticoids On Macrophage

The genomic mechanism of GC has been accepted widely. However, more evidence suggests that GC may exert nongenomic actions which are different from classic genomic effects. Many articles have reported nongenomic GC effects and explored the possible mechanisms, but most were in relation to neurons and endocrine cells. However, GCs are used clinically as anti-inflammatory and immunosuppressive drugs. To date, the nongenomic effect and possible mechanisms of the above-mentioned effects have not been reported. Macrophages play important roles in inflammation and the immune response. The present experiment selected mouse peritoneal macrophages as experimental cells to explore the nongenomic effects and possible mechanisms of GCs on phagocytosis and superoxide anion production.In present experiment, thioglycollate-induced peritoneal macrophages were separated and purified. The phagocytosis of macrophages was detected by the neutral red uptake assay. The PMA-stimulated superoxide anion was measured by cytochrome C reduction assay. Our results present the following:(1) 10~-4 mol/L and 10~-5mol/L CORT, METH, HYDR all rapidly inhibited phagocytosis by macrophages in less than 30min, and the inhibition of 10~-4mol/L was stronger than that of 10~-5mol/L; DEXA and 10~-6 mol/L CORT, METH, HYDR could not inhibit phagocytosis by macrophage.(2) 10~-4mol/L to 10~-10 mol/LCORT METH, HYDR and DEXA rapidly inhibited superoxide anion production by macrophages in less than 30min and the effect was more strong with the higher concentration of GC.(3) RU486 is the classic GCs-receptor antagonist which binds with GC-receptor and subsequently blocks the genomic effect. It is known that GCs trigger genomic events and the synthesis of specific proteins that are responsible for physiological...