国际药学研究杂志
國際藥學研究雜誌
국제약학연구잡지
INTERNATIONAL JOURNAL OF PHARMACEUTICAL RESEARCH
2014年
4期
456-460
,共5页
方松柏%李维熙%汪婷美%陈欢%李怡芳%何蓉蓉
方鬆柏%李維熙%汪婷美%陳歡%李怡芳%何蓉蓉
방송백%리유희%왕정미%진환%리이방%하용용
茶花提取物%糖负荷%α-葡萄糖苷酶
茶花提取物%糖負荷%α-葡萄糖苷酶
다화제취물%당부하%α-포도당감매
tea flower extract%camellia flower%glycemic load,α-glucosidase
目的:研究茶花提取物对实验性糖负荷小鼠糖吸收的抑制作用。方法雄性昆明种小鼠分为糖负荷模型组、阿卡波糖(6.25 mg/kg)对照组、茶花提取物150及300 mg/kg剂量组,每组8只小鼠。模型组分别以葡萄糖(2 g/kg)、蔗糖(4 g/kg)和淀粉(6 g/kg)灌胃建立3种糖负荷餐后高血糖模型,给药组小鼠糖负荷前1 d及30 min分别灌胃给予阿卡波糖或茶花提取物,检测糖负荷后不同时间小鼠的血糖水平,探讨茶花提取物对小鼠糖吸收的影响。采用酶标法检测茶花提取物对体外和小鼠小肠黏膜α-葡萄糖苷酶的抑制活性。结果茶花提取物(150和300 mg/kg)及阿卡波糖(6.25 mg/kg)对葡萄糖负荷小鼠血糖水平的影响无显著性差异,但能明显降低蔗糖负荷20 min时的小鼠血糖水平(P<0.05),能明显降低淀粉负荷20 min和40 min时小鼠血糖水平(P<0.05)。茶花提取物150和300 mg/kg对小鼠小肠黏膜α-葡糖苷酶活性的抑制率分别为18.8%和31.1%,茶花提取物对α-葡糖苷酶的体外抑制活性(IC50值)为1.50 mg/ml。结论茶花提取物能有效降低糖负荷后的血糖水平,其作用机制可能与抑制α-葡萄糖苷酶活性有关。
目的:研究茶花提取物對實驗性糖負荷小鼠糖吸收的抑製作用。方法雄性昆明種小鼠分為糖負荷模型組、阿卡波糖(6.25 mg/kg)對照組、茶花提取物150及300 mg/kg劑量組,每組8隻小鼠。模型組分彆以葡萄糖(2 g/kg)、蔗糖(4 g/kg)和澱粉(6 g/kg)灌胃建立3種糖負荷餐後高血糖模型,給藥組小鼠糖負荷前1 d及30 min分彆灌胃給予阿卡波糖或茶花提取物,檢測糖負荷後不同時間小鼠的血糖水平,探討茶花提取物對小鼠糖吸收的影響。採用酶標法檢測茶花提取物對體外和小鼠小腸黏膜α-葡萄糖苷酶的抑製活性。結果茶花提取物(150和300 mg/kg)及阿卡波糖(6.25 mg/kg)對葡萄糖負荷小鼠血糖水平的影響無顯著性差異,但能明顯降低蔗糖負荷20 min時的小鼠血糖水平(P<0.05),能明顯降低澱粉負荷20 min和40 min時小鼠血糖水平(P<0.05)。茶花提取物150和300 mg/kg對小鼠小腸黏膜α-葡糖苷酶活性的抑製率分彆為18.8%和31.1%,茶花提取物對α-葡糖苷酶的體外抑製活性(IC50值)為1.50 mg/ml。結論茶花提取物能有效降低糖負荷後的血糖水平,其作用機製可能與抑製α-葡萄糖苷酶活性有關。
목적:연구다화제취물대실험성당부하소서당흡수적억제작용。방법웅성곤명충소서분위당부하모형조、아잡파당(6.25 mg/kg)대조조、다화제취물150급300 mg/kg제량조,매조8지소서。모형조분별이포도당(2 g/kg)、자당(4 g/kg)화정분(6 g/kg)관위건립3충당부하찬후고혈당모형,급약조소서당부하전1 d급30 min분별관위급여아잡파당혹다화제취물,검측당부하후불동시간소서적혈당수평,탐토다화제취물대소서당흡수적영향。채용매표법검측다화제취물대체외화소서소장점막α-포도당감매적억제활성。결과다화제취물(150화300 mg/kg)급아잡파당(6.25 mg/kg)대포도당부하소서혈당수평적영향무현저성차이,단능명현강저자당부하20 min시적소서혈당수평(P<0.05),능명현강저정분부하20 min화40 min시소서혈당수평(P<0.05)。다화제취물150화300 mg/kg대소서소장점막α-포당감매활성적억제솔분별위18.8%화31.1%,다화제취물대α-포당감매적체외억제활성(IC50치)위1.50 mg/ml。결론다화제취물능유효강저당부하후적혈당수평,기작용궤제가능여억제α-포도당감매활성유관。
Objective To study the inhibitory effects of tea flower extract(TFE) onα-glucosidase and glucose intestinal absor-ption. Methods Three different postprandial hyperglycemia models (2 g/kg glucose, 4 g/kg sucrose, and 6 g/kg starch) were used, with 8 mice in each group. Oral administration of 150 or 300 mg/kg of TFE, 6.25 mg/kg of acarbose, or water was performed on mice 1 day and 30 mins before the oral administration of 2 g/kg glucose, 4 g/kg sucrose, and 6 g/kg starch at 10 ml/kg of body weight. Blood glucose levels were analyzed chronologically to evaluate the effect of TFE. In vitro studies were also performed to study the inhibitory effects of TFE on α-glucosidase and small intestinal mucosa glycosidase. Results Neither TFE nor acarbose had significant influence in glucose-treated mice. However, there was a significant decrease in the postprandial blood glucose 20 min after sucrose administration (P<0.05), and 20 min and 40 min after starch administration (P<0.05). TFE also significantly inhibited the activities ofα-glucosidase of small intestinal mucosa, with 18.8%and 31.1%by 150 and 300 mg/kg TFE. The in vitro IC50 of TFE onα-glucosidase was 1.50 mg/ml. Conclusion TFE could effectively reduce the blood glucose level in hyperglycemic mice. Its mechanism might be related to the inhibitory effects ofα-glucosidase.