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Objective To investigate effects of endotoxin on 11?-HSD2 gene transcription in vascular endothelial cells to observe the role of p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway. Methods The effects of endotoxin in the presence or absence of p38 MAPK specific inhibitor SB203580 on the transcription of 11?-HSD2 in vascular endothelial cells was evaluated by reverse transcription DNA polymerase chain reaction. Results Treatments of endotoxin (1.0, 10, 20, 50, 100 ?g/ L) for 24 h increased the ratios of 11?-HSD2mRNA/?-actin mRNA in vascular endothelial cells. The induction of 11?-HSD2 mRNA by endotoxin could be inhibited partially by 10 mmol/ L SB203580. Conclusion Endotoxin stimulated the transcription of 11?-HSD2 gene in vascular endothelial cells. The activation of p38 MAPK might be an important mechanism of 11?-HSD2 gene induced by endotoxin.
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Objective To investigate the effect of dexamethasone (Dex) on the transcription of 11 ?-hydroxysteroid dehydrogenase type 1 (11?-HSD1) gene in vascular endothelial cells. The roles of p38 mitogen-activated protein kinase (p38MAPK) signaling pathway and glucocorticoid receptor (GR) were also observed. Methods Vascular endothelial cells were co-cultured with different concentrations of Dex (10-9-10-3mol/L) for 24h. Reverse transcription polymerase chain reaction (RT-PCR) was employed to detect 11?-HSD1 mRNA in each group. Normally cultured cells, without contact with Dex, served as normal control group. The cells were co-cultured with p38MAPK specific inhibitor SB20358 (10-2mol/L) and GR specific inhibitor RU486 (10-6mol/L) for 24h, then RT-PCR was employed to detect 11?-HSD1 mRNA in each group. Among the groups, Dex-treated cells and non-intervened cells were grouped as negative control and normal control, respectively. Results 11?-HSD1 mRNA/?-actin mRNA of Dex-treated groups (respectively as 0.120?0.040, 0.140?0.020, 0.280?0.030, 0.360?0.060, 0.460?0.040) were significantly higher than that of the normal control (0.030?0.004, P
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Objective To explore the protection mechanism of glucocorticoids (GC) against the inflammatory injury of vascular endothelial cells (VEC). Methods An inflammatory injury model of VEC was reproduced by treating the human umbilical vein endothelial cells (HUVEC) with lipopolysaccharides (LPS) in vitro. The effect of dexamethasone (Dex) on apoptosis of HUVEC and the release of IL-6 and sICAM-1 of HUVEC was observed, and then the effect of RU486 (an antagonist for glucocorticoid receptor) on reversing the effect of Dex was also observed. Results LPS could induce apoptosis of HUVEC, and the apoptosis rate reached 36.7%?3.9%. On the other hand, glucocorticoid (Dex) could obviously inhibit the apoptosis of HUVEC in LPS, and the apoptosis rate was reduced to 13.2%?0.9%. The difference between the apoptosis rate between these two groups was very significant (P