Gao Jian Ping, Chen Chang Xun, Wang Ying, Lü Jian, Gu Wei Liang
Department of Pharmacology, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
J Pharm Pharmacol. 2009 May;61(5):677-83. doi: 10.1211/jpp/61.05.0018.
The aim of the study was to determine the effect of sodium houttuyfonate on myocardial hypertrophy and its mechanism of action in mice and rats.
A mouse model of myocardial hypertrophy was established by subcutaneous injection with isoproterenol. Mice were randomly divided into five groups: normal control; isoproterenol control; isoproterenol plus metoprolol; isoproterenol plus low- and high-dose sodium houttuyfonate. A rat model of myocardial hypertrophy was established by intraperitoneal injection with L-thyroxine. Rats were randomly divided into five groups: normal control; L-thyroxine control; L-thyroxine plus captopril; L-thyroxine plus low- and high-dose sodium houttuyfonate. At the end of the experiments, the left ventricular weight index and heart weight index were determined in mice and rats, the size of cardiomyocytes was measured in rats and the concentrations of cAMP in plasma and angiotensin II in ventricular tissue of mice were detected by radioimmunoassay. The endothelin-1 concentration was measured by radioimmunoassay and the hydroxyproline content was measured by a digestive method in ventricular tissue of rats.
After 7-9 days of treatment, sodium houttuyfonate significantly reduced the left ventricular weight index and heart weight index in mice and rats with myocardial hypertrophy, decreased the size of cardiomyocytes in rats, and reduced the content of cAMP and angiotensin II in mice with myocardial hypertrophy. It also decreased the endothelin-1 concentration and the hydroxyproline content in ventricular tissue in rats.
Sodium houttuyfonate can inhibit myocardial hypertrophy in mouse and rat models by restricting the activity of the sympathetic nervous system and decreasing the levels of angiotensin II and endothelin-1 in ventricular tissue.
本研究旨在确定鱼腥草素钠对小鼠和大鼠心肌肥大的影响及其作用机制。
通过皮下注射异丙肾上腺素建立小鼠心肌肥大模型。将小鼠随机分为五组：正常对照组；异丙肾上腺素对照组；异丙肾上腺素加美托洛尔组；异丙肾上腺素加低剂量和高剂量鱼腥草素钠组。通过腹腔注射L-甲状腺素建立大鼠心肌肥大模型。将大鼠随机分为五组：正常对照组；L-甲状腺素对照组；L-甲状腺素加卡托普利组；L-甲状腺素加低剂量和高剂量鱼腥草素钠组。实验结束时，测定小鼠和大鼠的左心室重量指数和心脏重量指数，测量大鼠心肌细胞大小，并通过放射免疫分析法检测小鼠血浆中cAMP浓度和心室组织中血管紧张素II浓度。通过放射免疫分析法测定大鼠心室组织中内皮素-1浓度，采用消化法测定大鼠心室组织中羟脯氨酸含量。
治疗7-9天后，鱼腥草素钠显著降低了心肌肥大小鼠和大鼠的左心室重量指数和心脏重量指数，减小了大鼠心肌细胞大小，降低了心肌肥大小鼠血浆中cAMP和心室组织中血管紧张素II的含量。它还降低了大鼠心室组织中内皮素-1浓度和羟脯氨酸含量。
鱼腥草素钠可通过抑制交感神经系统活性并降低心室组织中血管紧张素II和内皮素-1水平来抑制小鼠和大鼠模型中的心肌肥大。
