桂皮醛对糖尿病小鼠血糖水平的影响及机制  

Effect and Mechanism of Cinnamaldehyde on Insulin Resistance in db/db Mice

作　　者：黄链莎[1] 刘铜华[2] 孙文[2] 许光远 郭璇[2] 李迎真[1] 陈淑惠[1] 周鹏[1] HUANG Lian-sha;LIU Tong-hua;SUN Wen;XU Guang-yuan;GUO Xuan;LI Ying-zhen;CHEN Shu-hui;ZHOU Peng(Baoan District Hospital of Traditional Chinese Medicine, Shenzhen 518133, China;Key Laboratory of Health Cultivation of the Ministry of Education, Beijing University of Chinese Medicine, Beijing 100029, China;Fuxing Hospital, Capital Medical University, Beijing 100045, China)

机构地区：[1]深圳市宝安区中医院,深圳518133 [2]北京中医药大学教育部中医养生学重点实验室,北京100029 [3]首都医科大学附属复兴医院,北京100045

出　　处：《中国实验方剂学杂志》2018年第10期95-100,共6页Chinese Journal of Experimental Traditional Medical Formulae

基　　金：国家自然科学基金项目(81503550);广东省自然科学基金项目(2015A030310222)

摘　　要：目的：观察桂皮醛（cinnamaldehyde,CA）降血糖作用,并探讨其作用机制。方法：6~8周龄雄性db/db小鼠24只,按血糖随机分为模型组,二甲双胍组（0.2 g·kg^-1）,桂皮醛低剂量组（0.025 g·kg^-1）和桂皮醛高剂量组（0.05 g·kg^-1）,每组6只,另设同周龄C57BL/6J小鼠6只为正常组。治疗4周后,检测各组小鼠空腹血糖（fasting blood glucose,FBG）,总胆固醇（total cholesterd,TC）,甘油三酯（total triglyceride,TG）,游离脂肪酸（free fatty acids,FFA）,天门冬氨酸氨基转移酶（aspartate aminotransferase,AST）,血清胰岛素（fasting insulin,Fins）水平,计算胰岛素抵抗指数（homa insulin-resistance,HOMA-IR）;取肝脏组织检测肝糖原含量以及高碘酸-希夫（periodic acid-Schiff stain,PAS）染色;采用实时荧光定量聚合酶链式反应（Real-time PCR）,蛋白免疫印迹法（Western blot）检测肝脏相关mRNA和蛋白表达。结果：治疗4周后,与模型组比较,CA组小鼠体质量,FBG,Fins,HOMA-IR,血脂明显降低（P〈0.05,P〈0.01）,肝脏糖原含量显著升高;小鼠肝脏葡萄糖-6-磷酸酶（glucose-6-phosphate,G-6-P）,磷酸烯醇式丙酮酸羧激酶（phosphoenolpyruvate carboxykinase,PEPCK）mRNA表达显著降低（P〈0.01）,p-蛋白激酶B（protein kinase B,Akt）,p-糖原合成酶激酶-3β（GSK-3β）蛋白表达显著升高（P〈0.01）。结论：CA具有降低血糖作用,相关机制可能是通过上调肝脏胰岛素信号通路Akt,GSK-3β磷酸化水平,抑制G-6-P,PEPCK mRNA表达实现。Objective：To elucidate the effect and mechanism of cinnamaldehyde（CA） in improving blood glucose in obese db/db mice.Method：Twenty-four 6 to 8-week-old male db/db mice were randomly divided into model group,Metformin group,low-dose CA group and high-dose CA group according to their levels of blood glucose,with 6 in each group,while six C57 BL/6 J mice of the same age were included in normal group.After treatment for four weeks,fasting blood glucose（FBG）,total cholesterd（TC）,total triglyceride（TG）,free fatty acids（FFA）,aspartate aminotransferase（AST）,fasting insulin（Fins）,homa insulin-resistance（HOMA-IR）,hepatic glycogen and PAS staining of liver were measured.Real-time PCR and Western blot were used to quantify the mRNA and protein expressions of certain targets in liver.Result：It was found that the body weight,fast blood glucose,Fins,HOMA-IR,lipid were significantly decreased in the CA group compared with model group after the treatment for 4 weeks（P〈0.05,P〈0.01）.Hepatic glycogen was higher in the CA group than model group（P〈0.01）.The mRNA expressions of glucose-6-phosphate（G-6-P）,phosphoenolpyruvate carboxykinase（PEPCK） in mice of CA group decreased significantly（P〈0.01）,and the protein expressions of p-protein kinase B（Akt）,p-glycogenkinase3β（GSK3β） in mice of CA group increased significantly（P〈0.01）.Conclusion：It was demonstrated that CA may reduce the blood glucose in db/db mice by up-regulating the mRNA expressions of G-6-P and PEPCK,and down-regulating the protein expressions of p-Akt,p-GSK3β in liver.

关 键 词：桂皮醛 2型糖尿病 葡萄糖-6-磷酸酶(G-6-P)/磷酸烯醇式丙酮酸羧激酶(PEPCK) 蛋白激酶B(Akt)/糖原合成酶激酶-3β(GSK-3β) 

分 类 号：R22[医药卫生—中医基础理论] R2-031[医药卫生—中医学]