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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: To investigate the regulatory effect of genistein on vasoactive substances in rats and its mechanism of action in inhibiting hypoxic pulmonary hypertension and pulmonary vascular remodeling. Methods: Male Wistar rats were randomly divided into 3 groups: normoxic control group (C), chronic hypoxia group (H) and chronic hypoxia + genistein group (H + G) And H + G group were placed in the decompression chamber to simulate altitude 5000m plateau for 8h / d for 21 days. Blood levels of nitric oxide (NO), endothelin (ET-1), prostacyclin (PGI2) Diol (E2), superoxide dismutase (SOD) and malondialdehyde (MDA) content. Results: Genistein could significantly inhibit the production of ET-1 and MDA, promote the production of NO and prostacyclin and increase the activity of SOD. Compared with plain control group and simple hypoxia group, there was no significant difference in serum estrogen level in genistein group. Conclusion: Genistein can regulate endothelium - dependent vasorelaxation / vasoconstrictor activity, enhance vasodilatation and inhibit the proliferation of vascular smooth muscle cells in order to achieve the prevention and treatment of chronic hypoxic pulmonary hypertension and pulmonary vascular remodeling. Genistein had no significant effect on estrogen levels in male rats, which could avoid the carcinogenesis of female and female uterus caused by estrogen and long-term use of estrogen.