RESUMEN
Objective To determine the effect of losartan on vascular remodeling and the underlying mechanism in spontaneously hypertensive rats(SHR). Methods SHR of 12 weeks old were given losartan orally [0,15,30 mg/(kg·d),n=12]. The tail arterial pressure was measured every week.Eight weeks later, the pathological changes and p22phox expression in the thoracic aorta, the activity of catalase (CAT), the contents of H2O2 and AngⅡ in the plasma were evaluated. Results Blood pressure was increased in the SHR accompanied by the thickened wall and increased p22phox expression in the thoracic aorta. The plasma levels of H2O2 and AngⅡwere elevated while the CAT level was decreased in the SHR. Administration of losartan reversed the thickened wall and increased the CAT activity concomitantly with the decreased plasma levels of H2O2 and p22phox expression in the SHR. The plasma level of AngⅡincreased after the losartan treatment. Conclusion Oxidative stress induces the vascular remodeling of the aorta in the SHR. Losartan can reverse the vascular remodeling through down-regulating p22phox expression and inhibiting the oxidative stress.
RESUMEN
Objective To investigate the effect of prostaglandin E1(PGE1) on the expression of monocyte chemoattractant protein-1(MCP-1)in human umbilical vein endothelial cells (HUVECs) and its possible mechanism. Methods Endothelial cells were incubated with oxidized low-density lipoprotein (ox-LDL group) in the presence or absence of prostaglandin E1. The level of MCP-1 in the supernatants was determined by enzyme linked immunosorbent assay (ELISA), the expression of MCP-1 mRNA in cultured endothelial cells was detected by in-situ hybridization and the protein expression of NF-κB was analyzed by Western blot. Results Compared with ox-LDL(100 μg/ml),PGE1 markedly lowered the levels of MCP-1[(0. 327±0. 051),(0. 214±0. 213),(0. 247±0. 228)pg/ml vs. (0. 655±0. 013)pg/ml], inhibiting the expression of MCP-1 mRNA [(0. 061±0. 008), (0. 033±0. 006),(0. 026±0. 004)A/μm2 vs. (0. 220±0. 032)A/μm2] in the cultured HUVECs in a dosedependent manner (0. 001, 0. 01, 0.1 mol/L). Western blot analysis demonstrated that the amount of NF-κB p65 was attenuated after treatment with prostaglandin E1 for 24 hours. Conclusions Prostaglandin E1 can downregulate the expressions of MCP-1 and NF-κB induced by ox-LDL in HUVECs, which may thereby defend the blood vessel endothelial cell function.