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作 者:汤旭蓁[1] 关腾[1] 钱贻崧[1] 李运曼[1] 孙宏斌[2] 黄景慧[3] 章宇[3]
机构地区:[1]中国药科大学生理教研室 [2]中国药科大学新药研究中心 [3]中国药科大学基础药学理科基地,南京210009
出 处:《中国天然药物》2008年第1期53-56,共4页
基 金:教育部"2005年度新世纪优秀人才支持计划"资助项目(NCET-05-0495);高等学校博士学科点专项科研基金资助项目(Y051018)~~
摘 要:目的:考察糖原磷酸化酶抑制剂山楂酸对正常和实验性高血糖模型小鼠的降血糖作用及对肝糖原的影响,初步探讨其降糖机制。方法:山楂酸灌胃7天,分别以皮下注射肾上腺素,口服葡萄糖造成小鼠高血糖模型,与正常组一起测定静脉血糖和肝糖原含量。结果:山楂酸可显著对抗肾上腺素、葡萄糖引起的血糖升高,对抗肾上腺素引起的肝糖原降解,增加葡萄糖致高血糖小鼠肝糖原含量;可增加正常小鼠肝糖原储备,但不影响正常血糖。结论:山楂酸具有降血糖作用,机制与其抑制肝糖原分解有关。AIM: To determine the effects of maslinic acid, a novel glycogen phosphorylase inhibitor, on blood glucose and hepatic glycogen in normal and hyperglycemia mice and investigate its mechanism. METHODS: Mice were given intragastrically either vehicle or maslinic acid for 7 days. The model of hyperglycemia in mice was set up by subcutaneous injection of adrenaline or intragastric administration of glucose respectively; the fasting plasma glucose and hepatic glycogen of both normal and hyperglycemia mice were measured. RESULTS- The elevation of blood glucose level caused by adrenaline or glucose was antagonized by maslinic acid significantly. Maslinic acid also increased the hepatic glycogen content in both adrenaline and glucose - induced hyperglycemia mice. Maslinic acid showed no significant effect on fasting plasma glucose level while increased the hepatic glycogen content of normal mice. CONCLUSION: Maslinic acid presents anti- diabetic effect, the mechanism is probably concerned with inhibiting excessive hepatic glycogen degradation.
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