Ernsberger Paul, Johnson Janean L, Rosenthal Talma, Mirelman David, Koletsky Richard J
Department of Nutrition, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4906, USA.
Am J Hypertens. 2007 Aug;20(8):866-74. doi: 10.1016/j.amjhyper.2007.02.015.
Hypertension often coexists with hyperlipidemia, insulin resistance, and glucose intolerance in metabolic syndrome. Allylmercaptocaptopril is a conjugate of the angiotensin-converting enzyme inhibitor captopril with allicin, an active principle in garlic with multiple beneficial actions on metabolic-syndrome abnormalities. We sought to test the hypothesis that the conjugation of allicin to captopril may confer additional therapeutic actions in metabolic disease.
We compared allylmercaptocaptopril (53.5 mg/kg/day orally for 60 days) to an equimolar dose of captopril (40 mg/kg/day) in the spontaneously hypertensive, obese rat (SHROB) model.
Allylmercaptocaptopril prevented progressive weight gain, without a detectable effect on food intake. Both captopril and allylmercaptocaptopril lowered blood pressure, but allylmercaptocaptopril was more effective. Allylmercaptocaptopril, but not captopril, improved cardiac hypertrophy, as indicated by heart weight and ventricular-wall thickness. Allylmercaptocaptopril improved, whereas captopril impaired, oral glucose tolerance after a fast. Triglycerides were decreased by both captopril and allylmercaptocaptopril. Total cholesterol and non-HDL cholesterol were reduced by captopril but not by allylmercaptocaptopril. The SHROB rats developed severe glomerulosclerosis and renal failure. Allylmercaptocaptopril showed significant nephro-protection, as indicated by reductions in urinary protein loss, urinary protein-to-creatinine ratio, and plasma creatinine. Captopril showed the same trends and also prevented the decline of creatinine clearance. Finally, both allylmercaptocaptopril and captopril reduced the basal level of lipolysis in isolated abdominal adipocytes, and restored the response to catecholamine stimulation.
Both captopril and allylmercaptocaptopril are effective in attenuating multiple abnormalities of metabolic syndrome. Allylmercaptocaptopril may have additional effectiveness on improving glucose tolerance, further lowering blood pressure, reducing cardiac hypertrophy, preventing weight gain, and protecting against renal disease.
高血压常与代谢综合征中的高脂血症、胰岛素抵抗和葡萄糖耐量异常并存。烯丙基巯基卡托普利是血管紧张素转换酶抑制剂卡托普利与大蒜素的共轭物,大蒜素是大蒜中的一种活性成分,对代谢综合征异常具有多种有益作用。我们试图验证大蒜素与卡托普利的共轭可能在代谢性疾病中赋予额外治疗作用这一假设。
在自发性高血压肥胖大鼠(SHROB)模型中,我们将烯丙基巯基卡托普利(口服53.5毫克/千克/天,持续60天)与等摩尔剂量的卡托普利(40毫克/千克/天)进行比较。
烯丙基巯基卡托普利可防止体重逐渐增加,对食物摄入量无明显影响。卡托普利和烯丙基巯基卡托普利均可降低血压,但烯丙基巯基卡托普利更有效。如心脏重量和心室壁厚度所示,烯丙基巯基卡托普利可改善心脏肥大,而卡托普利则无此作用。烯丙基巯基卡托普利可改善禁食后的口服葡萄糖耐量,而卡托普利则会损害口服葡萄糖耐量。卡托普利和烯丙基巯基卡托普利均可降低甘油三酯水平。卡托普利可降低总胆固醇和非高密度脂蛋白胆固醇水平,而烯丙基巯基卡托普利则无此作用。SHROB大鼠出现严重的肾小球硬化和肾衰竭。烯丙基巯基卡托普利显示出显著的肾脏保护作用,表现为尿蛋白丢失、尿蛋白与肌酐比值及血浆肌酐降低。卡托普利也呈现相同趋势,且还可防止肌酐清除率下降。最后,烯丙基巯基卡托普利和卡托普利均可降低分离的腹部脂肪细胞的基础脂肪分解水平,并恢复对儿茶酚胺刺激的反应。
卡托普利和烯丙基巯基卡托普利均可有效减轻代谢综合征的多种异常。烯丙基巯基卡托普利在改善葡萄糖耐量、进一步降低血压、减轻心脏肥大、防止体重增加和预防肾脏疾病方面可能具有额外的疗效。