摘要
目的:探讨染料木黄酮对大鼠血管活性物质的调节作用,以了解其抑制缺氧性肺动脉高压及肺血管结构改建的作用机制。方法:将雄性Wistar大鼠随机分为3组,常氧对照组(C)、慢性缺氧组(H)和慢性缺氧+染料木黄酮组(H+G),C组在平原,H组和H+G组置于减压舱,模拟海拔5000m高原,8h/d,持续21d,分别检测血中一氧化氮(NO)、内皮素(ET-1)、前列环素(PGI2)、雌二醇(E2)、超氧化物歧化酶(SOD)及丙二醛(MDA)的含量。结果:染料木黄酮可以显著抑制ET-1和MDA的产生,促进NO和前列环素的生成,提高SOD活性。与平原对照组和单纯缺氧组比较,染料木黄酮组大鼠血清雌激素水平无显著差异。结论:染料木黄酮可以调节内皮依赖性舒血管/缩血管活性物质的平衡,加强血管舒张作用,抑制血管平滑肌细胞增殖,从而实现对慢性缺氧性肺动脉高压和肺血管结构改建防治作用。染料木黄酮对雄性大鼠体内雌激素水平无显著影响,可以避免长期使用雌激素产生的女性乳腺和子宫的癌变及男性雌化等不良反应。
Objective： The regulative effects of genistein on vascular active factors, to find its mechanism to suppressed pulmonary hypertension and vascular structural remodeling, were discussed in chronic hypoxic rats. Methods： Male Wistar rats were randomly divided into control group （C）, hypoxia group （H） and hypoxia with genistein group （H＋G）. Control group of rats was kept in cages exposed to room air. H and （H＋G） groups of rats were exposed to 21 days of hypobaric hypoxia（simulate altitude 5000m）for 8h everyday. During their esposure to hypoxia, rats were i.g. administered once a day with solvent or phytoestrogens. The levels of nitric oxide（NO）, endothelin （ET-1）, prostacyclin （PGI2）, 17 β -estradiol （E2）, superoxide dismutase（SOD） and malondialdehyde （MDA） of blood were measured. Results： Genistein could increase NO and PGI2, and decrease ET-1 levels and also be responsible for genistein induced vasodilation. In addition, genistein could increase the activity of SOD and inhibit MDA product. Serum 17 β -estradiol levels were not significantly different among rats in three groups. Conclusions： Genistein could suppress SMC proliferation by inhibiting the synthesis and secretion of ET-1 and other SMC proliferation-promoting factors, and enhancing the synthesis and secretion of SMC proliferation-inhibitory factors, such as NO and PGI2. Genistein did not have the side effects, such as feminizing and oncogenic effects, of the estrogens.
出处
《食品科学》
EI
CAS
CSCD
北大核心
2005年第10期219-223,共5页
Food Science
