Hypoglycemic effect of Ganoderma lucidum polysaccharides

作     者：Hui-na ZHANG,Zhi-binLIN2 Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing 100083, China 

作者机构：Department of Pharmacology School of Basic Medical Sciences Peking University 

出 版 物：《Acta Pharmacologica Sinica》 (中国药理学报(英文版))

年 卷 期：2004年第25卷第2期

页      面：65-69页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 100602[医学-中西医结合临床] 10[医学] 

基　　金：Project supported by Research Fund of Shanghai Green Valley Holding Co  Ltd 

主　　题：Ganoderma lucidum polysaccharides hypoglycemic agents glucose insulin calcium pancreas 

摘      要：AIM: To investigate the hypoglycemic effect of Ganoderma lucidum polysaccharides (Gl-PS) in the normal fasted mice and its possible mechanism. METHODS: Normal fasted mice were given a single dose of Gl-PS 25, 50, and 100 mg/kg by ip and the serum glucose was measured at 0, 3, and 6 h after administration. Gl-PS 100 mg/kg were also given by ip and the serum glucose and insulin levels were measured at 0 min, 30 min, 1 h, 3 h, 6 h, and 12 h. Pancreatic islets were isolated and incubated with glucose 5.6 mmol/L and different concentration of Gl-PS, the insulin content of islets and insulin release were examined. The islets fluorescent intensity of [Ca2+]i was also studied with a confocal microscope. Verapamil and egtazic acid were used to testify whether the insulin-releasing effect of Gl-PS was mediated by its ability to raise the Ca2+ influx. RESULTS: Gl-PS dose-dependently lowered the serum glucose levels at 3 h and 6 h after administration. Gl-PS 100 mg/kg raised the circulating insulin levels at 1 h after administration. In vitro, Gl-PS had no effect on islets insulin content, but it stimulated the insulin release after incubation with glucose 5.6 mmol/L. Confocal microscope showed that Gl-PS 100 mg/L had the capacity to raise the [Ca2+] i. The insulin-releasing effect of Gl-PS was inhibited by verapamil/egtazic acid. CONCLUSION: Gl-PS possesses the hypoglycemic effect on normal mice; one mechanism is through its insulin-releasing activity due to a facilitation of Ca2+ inflow to the pancreatic β cells.