The purpose of the present study was to investigate the effect of 17beta-estradiol (17beta-E(2)) on the structure and relaxation and contraction activity of thoracic aortas in ovariectomized rats with
insulin resistance induced by
fructose. Ovariectomized mature female Sprague-Dawley rats were fed with high
fructose diet for 8 weeks to induce
insulin resistance. Physiological dose of 17beta-E(2) (30 mug/kg) was injected subcutaneously every day for 8 weeks. Systolic blood pressure (SBP) was measured by use of tail-cuff. Serum
nitric oxide (NO),
estradiol (E(2)), fasting
blood sugar (FBS) and fasting serum
insulin (FSI) were measured respectively in each group. The
insulin sensitive index (ISI) was calculated. The thoracic aortas were fixed in
formalin, sliced and HE dyed. The structure of thoracic aortas, lumen breadth, media thickness, media thickness/lumen breadth ratio and media cross-section area were measured. The contraction response of thoracic aorta rings induced by L-
phenylephrine (PE) and the relaxation response of thoracic aorta rings induced by ACh and
sodium nitroprusside (SNP) were measured. To explore the mechanism,
nitric oxide synthase (NOS) inhibitor N-nitro-
L-arginine methyl ester (
L-NAME) was used. The results obtained are as follows: (1) 17beta-E(2) protected against the effect of high
fructose diet, which caused an increase in SBP,
hyperinsulinemia and a decrease in ISI in ovariectomized rats. (2) The structure of thoracic aortas had no significant difference among the groups. (3) Compared with the ovariectomized group (OVX) or
fructose fed group (F), serum
nitric oxide was significantly reduced, the contraction response of thoracic aorta rings to PE was enhanced and the relaxation response to ACh was depressed significantly in ovariectomized+fructose fed group (OVX+F). The effect of high
fructose was reversed by 17beta-E(2). After pretreatment with
L-NAME, the effect of 17beta-E(2), which enhanced the relaxation response of thoracic aorta rings to ACh in ovariectomized+
fructose+17beta-E(2) group (OVX+F+E(2)), was partly blocked. (4) The relaxation response of thoracic aorta rings to SNP had no significant difference among the groups. (5) The contraction response of thoracic aorta rings without endothelium to PE had no significant difference among the groups. These findings suggest that 17beta-E(2) may provide protection against the effect of high
fructose diet, which causes
hypertension, dysfunction of endothelial cells and
insulin resistance. The mechanism of this effect of 17beta-E(2) could be partly associated with the increase of NO by NOS pathway, or associated with the decrease in the level of systolic blood pressure and serum
insulin, and the improvement of
insulin resistance.