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甘草甜素对大鼠血压的影响及其机制 |
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张永生 吴平生 刘伊丽 王煊 梁欣伟 郭志刚 赖文岩
【摘要】 目的 探讨甘草甜素通过抑制11β羟化固醇脱氢酶2型催化活性导致血压升高及其机制。方法 对9只及6只Wistar大鼠给予外源性甘草甜素5周及3个月后观察血压变化，光镜检查心脏及主动脉的滋养动脉的病理改变，观察肠系膜动脉对去甲肾上腺素加压反应，并通过肠系膜血管网的离体灌注，检测灌注液中皮质醇及醛固酮的含量，通过RT-PCR观察甘草甜素处理大鼠主动脉11β-羟化固醇脱氢酶2型及醛固酮合成酶mRNA表达的变化。结果 甘草甜素使大鼠血压升高，心脏及主动脉的滋养动脉出现平滑肌细胞增生和肥大，血管壁增厚及玻璃样变性，肠系膜动脉对去甲肾上腺素的加压反应增高，肠系膜血管网灌注液中皮质醇含量增高及醛固酮含量减低，主动脉11β-羟化固醇脱氢酶2型及醛固酮合成酶mRNA的表达受抑。结论 提示甘草甜素通过抑制11β-羟化固醇脱氢酶2型及醛固酮合成酶mRNA的表达，导致局部组织皮质醇水平增高、醛固酮降低，增加血管平滑肌对去甲肾上腺素的反应性引起血压升高。
【关键词】 高血压 羟甾类脱氢酶类 甘草甜素
Effects of glycyrrhizin on blood pressure and its mechanisms ZHANG Yongsheng, WU Pingsheng, LIU Yili, et al. Department of Cardiology, Nanfang Hospital, First Military Medical University, Guangzhou 510515
【Abstract】 Objective To confirm the action of glycyrrhizin on blood pressure by inhibiting the activity of 11β-hydroxysteroid dehydrogenase type Ⅱ(11βHSD 2) and to test its mechanism. Methods Male Wistar rats and SHRs (weighing 150～220 g) were given glycyrrhizin (Sigma) 200 mg/kg /day, orally for 5 weeks and 3 months. The blood pressure was monitored by means of a pressure transducer connected to a polygraph and recorded. Histological pathological chages of the nutrient arteries of the heart and aorta were studied with light microscope. Mesenteric artery perfusion ex vivo and pressor responses to norepinephrine were performed. The perfusate from the mesenteric arteries was collected and used for reverse phase high performance liquid chromatography to measure aldosterone and corticosterone level. RT-PCR was used to measure the expression of 11βHSD 2 and aldosterone synthase (CYP11B2) mRNA.Results The results showed that the systolic blood pressure was significantly increased in Wistar rats treated with glycyrrhizin compared with those not treated. Hyperplasia of smooth muscle cells and hypertrophy in arterioles were observed under microscope. The pressor responses to norepinephrine in mesenteric arteries[1] [2] 下一页
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