[Protective effects of Astragalus membranaceus on free fatty acid-induced vascular endothelial cell dysfunction].

OBJECTIVE: To investigate whether Astragalus membranaceus (AM) can protect endothelium-dependent vasodilatation (EDV) function of aorta from the damage induced by high level of free fatty acid (FFA).

METHODS: Ten male SD rats, 8 weeks old and 250-300 g in weight, were sacrificed and thoracic aorta were harvested. Aorta rings incubated in organ baths were divided into three groups, Control group, FFA group and FFA+ AM group. The control group was incubated in 20 mL Krebs-Henseleit solution; the FFA group was incubated in 20 mL KH solution mixed with FFA(800 micromol/L) the FFA + AM group was incubated in 20 mL KH solution mixed with FFA (800 micromol/L) and AM (4 g/L). The relaxation levels of aorta rings response to acetylcholine and sodium nitroprusside were measured, the expression of NF-kappaB and the level of NOx in the organ bath were analyzed by immunohistochemistry.

RESULTS: Severe endothelial dysfunction were induced in FFA group (maximal vasorelaxation in response to Ach: 61.1% +/- l6.9% vs. 93.1% +/- 2.7% in control, P < 0.05), while EDV in FFA+AM group was significantly improved by the incubation with AM (P < 0.05). Compared with the control group (104.1 +/- 14.2) micromol/g, NOx levels of FFA group was (83.1 +/- 8.4) micromol/g (P < 0.05), and the treatment of AM increased the levels of NOx (98.8 +/- 10.7) micromol/g (P < 0.05). The control vascular ring had a little NF-kappaB expression in endothelial nucleus, FFA increased the activation of NF-kappaB, while the treatment of AM lower the elevated NF-kappaB level.

CONCLUSION: FFA can directly injure EDV, while AM may ameliorate it, with the possible mechanism related to the signal pathway of NF-kappaB and NO.