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蛇菰乙醇提取物降血糖作用的实验研究
引用本文:田金英,吉腾飞 苏亚伦,丛维娜,刘子良,叶菲.蛇菰乙醇提取物降血糖作用的实验研究[J].中国中药杂志,2007,32(12):1194-1198.
作者姓名:田金英  吉腾飞 苏亚伦  丛维娜  刘子良  叶菲
作者单位:中国医学科学院,中国协和医科大学,药物研究所,北京,100050
基金项目:国家自然科学基金;国家中医药管理局科研项目
摘    要:目的:探讨蛇菰95%乙醇提取物(SHG)的降血糖作用及其机制。方法:以四氧嘧啶诱导雄性ICR小鼠形成糖尿病模型。用葡萄糖氧化酶法测定血糖浓度,用同位素放射免疫法测定血清胰岛素浓度。给动物口服SHG相当于生药20,30 g·kg-1体重连续7~10 d,以动物不禁食和禁食2.5 h的血糖水平和口服葡萄糖负荷后的血糖水平,观察SHG对机体血糖及糖耐量的影响;以腹腔注射葡萄糖负荷后的血糖和血胰岛素水平,评价SHG对机体高血糖诱导血胰岛素水平的影响;以口服蔗糖耐量和口服淀粉耐量评价药物对糖吸收的影响。结果:SHG可显著降低正常和糖尿病小鼠的餐后血糖和空腹血糖水平。动物口服蔗糖和口服淀粉耐量实验中,SHG可明显降低并后移蔗糖或淀粉负荷后的血糖峰值,减少血糖-时间曲线下面积(AUC)。动物口服葡萄糖耐量实验中,SHG可显著降低葡萄糖负荷后血糖的峰值,减少AUC。在正常小鼠腹腔注射葡萄糖耐量实验中,SHG组平均血糖上升百分数明显低于对照组,但血胰岛素水平与对照组无明显差异。结论:SHG显著降低正常和糖尿病小鼠的餐后血糖和空腹血糖、改善葡萄糖耐量。SHG控制血糖作用的机制可能与抑制肠道α-葡萄糖苷酶和增强体内葡萄糖代谢有关。

关 键 词:蛇菰提取物(SHG)  血糖  葡萄糖耐量  α-葡萄糖苷酶
文章编号:1001-5302(2007)12-1194-05
收稿时间:2006-11-05
修稿时间:2006-11-05

Studies on hypoglycemic effect of extract of Balaophora polyandra in mice
TIAN Jin-ying; JI Teng-fei; SU Ya-lun; CONG Wei-na; LIU Zi-liang; YE Fei.Studies on hypoglycemic effect of extract of Balaophora polyandra in mice[J].China Journal of Chinese Materia Medica,2007,32(12):1194-1198.
Authors:TIAN Jin-ying; JI Teng-fei; SU Ya-lun; CONG Wei-na; LIU Zi-liang; YE Fei
Institution:Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Abstract:OBJECTIVE: To study the hypoglycemic effect of the extract of B. polyandra (SHG). METHOD: The diabetic mice were induced by alloxan in ICR mice. The blood glucose concentration was measured by glucose oxidase method. The serum insulin level was determined by 125I-insulin radioimmunoassay kit. The hypoglycemic effect was evaluated by the levels of both fasting and no-fasting blood glucose. The effect on serum insulin level was estimated by the values of the blood insulin and the changes of the blood glucose induced by the glucose intraperitoneal injection. The effect on the glucose absorption was investigated by the oral sucrose or starch tolerance test. RESULT: Both of the fasting and no-fasting blood glucose levels were decreased significantly by the treatment of 20 or 30 g raw materials crude drug x kg (-1) SHG orally for 7-10 d in ICR mice or in alloxan diabetic mice. In the oral sucrose tolerance test or oral starch tolerance test, the administration of SHG reduced significantly the peak value of the blood glucose and the area under the blood glucose-time curve (AUC) in normal or alloxan diabetic mice, respectively. These effects of SHG were similar to those of acarbose, a kind of alpha-glucosidase inhibitors. In the oral glucose tolerance test in normal and alloxan diabetic mice, SHG decreased both the blood glucose peak and the AUC induced by the glucose loading. But in the intraperitoneal injection glucose tolerance test the levels of insulin in both SHG and control mice were similar, however, the changes of the blood glucose level after the glucose-loading for 30 min in SHG mice was much lower than that in control mice. CONCLUSION: With the treatment of SHG, the fasting and no-fasting blood glucose concentrations were decreased and the glucose tolerance improved significantly in both normal and alloxan diabetic mice, and the inhibition of a-glucosidase might be one of its major mechanisms.
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