The Effect of Dehydroepiandrosterone on the Expression of AT_1 receptor and TNF-induced ICAM-1 in Va

来源 :South China Journal of Cardiology | 被引量 : 0次 | 上传用户:joy2000
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Objectives To further invest- igate the molecular mechanism of vasoprotective role of dehydroepiandrosterone (DHEA), we examined DHEA on AT1 receptor and ICAM-1 gene expression in vascular smooth muscle cells (VSMCs). Methods RT-PCR and Western Blot was used to determine the change of the expressions of mRNA and protein of AT1 and ICAM- 1 when given various concentration dehydroepian- drosterone. Results 1.AT1 was abundant under the basal condition. The expression of AT1 mRNA and protein decreased after stimulated by DHEA (at 10- 10mol/L , 10-8 mol/L, 10-6 mol/L) , and the effects of DHEA on AT1 protein was dose-dependent. ER inhibitor Tamoxifen and AR inhibitor Flutamide enhanced AT1 protein expression, but did not influence the mRNA expression. 2. The exp-ression of ICAM-1 gene was low under the basal condition.It increased when induced by TNF-α,but decreased when induced by DHEA (at 10-10 mol/L, 10-8 mol/L, 10-6 mol/L) , and the effects of DHEA on ICAM-1 gene expression were dose-dependent. Conclusions These findings suggest that DHEA modulates AT1 and inflammatory factor induced ICAM-1 gene expression in VSMC, but further studies are necessary in the mecha-nism of DHEA action. Objectives To further invest- igate the molecular mechanism of vasoprotective role of dehydroepiandrosterone (DHEA), we examined DHEA on AT1 receptor and ICAM-1 gene expression in vascular smooth muscle cells (VSMCs). Methods RT-PCR and Western Blot was used to determine The change of the expressions of mRNA and protein of AT1 and ICAM-1 when given various concentrations of dehydroepian-drosterone. Results 1. AT1 was abundant under the basal condition. The expression of AT1 mRNA and protein decreased after stimulated by DHEA (at 10- 10 mol / L, 10-6 mol / L), and the effects of DHEA on AT1 protein was dose-dependent. ER inhibitor Tamoxifen and AR inhibitor Flutamide enhanced AT1 protein expression, but did not affect the mRNA expression. When increased when induced by TNF-α, but decreased when induced by DHEA (at 10-10 mol / L, 10-8 mol / L , 10-6 mol / L), and the effects of DHEA on ICAM-1 gene expression were dose-d ependent. Conclusions These findings suggest that DHEA modulates AT1 and inflammatory factor-induced ICAM-1 gene expression in VSMC, but further studies are necessary in the mecha-nism of DHEA action.
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