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17#beta#--Estradiol protects against injury of aortic relaxation and contraction in ovariectomized rats with insulin resistance induced by fructose

Zhou Shouhong, Ling Hongyan, Tian Shaowen, Liu Xianqing, Wang Bingxiang, Hu Bi

Department of Physiology, School of Medicine, Nanhua University.Hengyang 421001,Hunan

Abstract

The purpose of the present study was to investigate the effect of 17#beta#-Estradiol (17#beta#-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 17#beta#-E_(2) (30 #mu#g /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) 17#beta#-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 nitricoxide 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 17#beta#-E_(2). After pretreatment with L-NAME, the effect of 17#beta#-E_(2), which enhanced the relaxation response of thoracic aorta rings to ACh in ovariectomized+fructose+17#beta#-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 17#beta#-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 17#beta#-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.

Key words: Estradiol;fructose;ovariectomized;insulin resistance;aorta;endothelium

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Zhou Shouhong, Ling Hongyan, Tian Shaowen, Liu Xianqing, Wang Bingxiang, Hu Bi. 17#beta#--Estradiol protects against injury of aortic relaxation and contraction in ovariectomized rats with insulin resistance induced by fructose. Acta Physiol Sin 2005; 57 (5): (in Chinese with English abstract).