Effect of high soy diet on the cerebrovasculature and endothelial nitric oxide synthase in the ovariectomized rat.

Effect of high soy diet on the cerebrovasculature and endothelial nitric oxide synthase in the ovariectomized rat.
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DOI:
10.1016/j.vph.2010.02.003
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发表时间:
2010-05
影响因子:
4
通讯作者:
Dorrance, Anne M.
Dorrance, Anne M.
中科院分区:
医学2区
文献类型:
--
作者:
Schreihofer, Derek A.;Deutsch, Christian;Lovekamp-Swan, Tara;Sullivan, Jennifer C.;Dorrance, Anne M.

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高大豆(HS)饮食是神经保护和促进血管扩张在周围。我们假设HS饮食可以通过模拟雌二醇对内皮型一氧化氮合酶(eNOS)系统的作用来促进脑血管血管扩张,包括增加eNOS的表达和降低caveolin-1的表达,从而增加一氧化氮(NO)的产生。去卵巢大鼠分别饲喂HS或无大豆饲粮(SF)±低生理性雌二醇(E2) 4周。E2和HS均未改变大脑中动脉(MCA)结构或血管对乙酰胆碱、血清素或苯肾上腺素的反应。雌二醇以enos依赖性的方式增强缓激素诱导的松弛。E2和HS虽然增加了脑和脑血管中eNOS mRNA的表达,但对MCA中eNOS蛋白的表达和磷酸化没有影响。然而,E2降低了MCA中的小窝蛋白-1蛋白。在MCAs中,E2和HS都没有改变雌激素受体(ER) α的表达,但E2确实降低了ER β的水平。这些数据表明,高脂饲料对血管no生成没有影响,E2可能通过降低NOS活性变构抑制剂caveolin-1的表达来调节基础no生成。然而,E2和HS对脑血管系统的影响很小,可能无法解释其在病理状态下的保护作用。
High soy (HS) diets are neuroprotective and promote vascular dilatation in the periphery. We hypothesized that a HS diet would promote vascular dilatation in the cerebrovasculature by mimicking estradiol's actions on the endothelial nitric oxide synthase (eNOS) system including increasing eNOS expression and decreasing caveolin-1 expression to increase nitric oxide (NO) production. Ovariectomized rats were fed HS or a soy-free diet (SF) ± low physiological estradiol (E2) for 4 weeks. Neither E2 nor HS altered middle cerebral artery (MCA) structure or vascular responses to acetylcholine, serotonin, or phenylephrine. Estradiol enhanced bradykinin-induced relaxation in an eNOS-dependent manner. Although E2 and HS increased eNOS mRNA expression in the brain and cerebrovasculature, they had no effect on eNOS protein expression or phosphorylation in the MCA. However, E2 decreased caveolin-1 protein in the MCA. In MCAs neither E2 nor HS altered estrogen receptor (ER) alpha expression, but E2 did reduce ER beta levels. These data suggest that HS diets have no effect on vascular NO production, and that E2 may modulate basal NO production by reducing the expression of caveolin-1, an allosteric inhibitor of NOS activity. However, the effects of E2 and HS on the cerebrovasculature are small and may not underlie their protective actions in pathological states.
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