Corticosterone rapidly promotes respiratory burst of mouse peritoneal macrophages via non-genomic mechanism  被引量:1

Corticosterone rapidly promotes respiratory burst of mouse peritoneal macrophages via non-genomic mechanism

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作  者:SHI Wen-lei MA Qian ZHANG Lu-ding HUANG Jun-long ZHOU Jian LIU Lei SHEN Xing-hua JIANG Chun-lei 

机构地区:[1]Laboratory of Stress Medicine, Department of Nautical Medicine, Second Military Medical University, Shanghai 200433, China [2]Department of Pediatrics, Chang-Zheng Hospital, Shanghai 200003, China

出  处:《Chinese Medical Journal》2011年第19期3127-3132,共6页中华医学杂志(英文版)

基  金:This work was supported by grants from the Military Twelfth Five-Year Plan and National Natural Science Foundation of China (No. 30873077, No. 30971083) The authors declared no conflicts of interests.

摘  要:Background The immunomodulatory effects of glucocorticoids (GCs) have been described as bimodal. High concentration of GCs exerts immunosuppressive effects and low levels of GCs are immunopermissive. While the immunosuppressive mechanisms of GCs have been investigated intensely, the immunopermissive effects of GCs remain unclear. A lot of studies showed GCs could exert rapid non-genomic actions. We herein studied the rapid immunopromoting effects of GCs.Methods We observed the rapid (within 30 minutes) effects of corticosterone on respiratory burst of mouse peritoneal macrophages and studied their mechanisms. The superoxide anions were measured by cytochrome C reduction assay.Protein kinase C phosphorylation was measured by Western blotting and membrane fluidity was evaluated by fluorescence polarization measurement.Results The 10-8 mol/L and 10-7 mol/L corticosterone rapidly increased the superoxide anions production by macrophages, which were insensitive to GC-receptor antagonist, mifepristone, and protein-synthesis inhibitor,cycloheximide. Corticosterone coupled to bovine serum albumin was able to mimic the effects of corticosterone. The effects were independent of protein kinase C pathway and the change in membrane fluidity.Conclusions The results indicate that corticosterone rapidly promote the superoxide anions production by mouse peritoneal macrophages may through non-genomic mechanisms. This study may contribute to understanding the effects of GCs under stress condition and the physiological significance of nongenomic effects of GCs.Background The immunomodulatory effects of glucocorticoids (GCs) have been described as bimodal. High concentration of GCs exerts immunosuppressive effects and low levels of GCs are immunopermissive. While the immunosuppressive mechanisms of GCs have been investigated intensely, the immunopermissive effects of GCs remain unclear. A lot of studies showed GCs could exert rapid non-genomic actions. We herein studied the rapid immunopromoting effects of GCs.Methods We observed the rapid (within 30 minutes) effects of corticosterone on respiratory burst of mouse peritoneal macrophages and studied their mechanisms. The superoxide anions were measured by cytochrome C reduction assay.Protein kinase C phosphorylation was measured by Western blotting and membrane fluidity was evaluated by fluorescence polarization measurement.Results The 10-8 mol/L and 10-7 mol/L corticosterone rapidly increased the superoxide anions production by macrophages, which were insensitive to GC-receptor antagonist, mifepristone, and protein-synthesis inhibitor,cycloheximide. Corticosterone coupled to bovine serum albumin was able to mimic the effects of corticosterone. The effects were independent of protein kinase C pathway and the change in membrane fluidity.Conclusions The results indicate that corticosterone rapidly promote the superoxide anions production by mouse peritoneal macrophages may through non-genomic mechanisms. This study may contribute to understanding the effects of GCs under stress condition and the physiological significance of nongenomic effects of GCs.

关 键 词:GLUCOCORTICOIDS MACROPHAGES superoxide anions respiratory burst NEUROIMMUNOMODULATION 

分 类 号:Q57[生物学—生物化学] Q691.5

 

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