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松茸多糖抑制高脂诱导的小鼠2型糖尿病机制研究 被引量:3

Mechanism of tricholoma matsutake polysaccharides inhibiting type 2 diabetes induced by high fat in mice
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摘要 目的:探讨松茸多糖(TMP)对小鼠2型糖尿病(T2DM)模型的干预作用,阐明TMP抗T2DM的作用机制。方法:利用超声-微波协同萃取法对松茸子实体提取物进行萃取得到TMP。采用高脂饮食诱导构建小鼠T2DM模型。将T2DM小鼠随机分为模型组(HFG组)、罗格列酮阳性对照组(Rosi组)、TMP低剂量组(TMP1组)和TMP高剂量组(TMP2组)。HFG组给予生理盐水灌胃,Rosi组给予罗格列酮灌胃,TMP1组和TMP2组给予TMP灌胃。采用实时荧光定量聚合酶链反应(qPCR)和Western Blot法检测小鼠肝组织中磷酸烯醇丙酮酸羧激酶(PEPCK)和葡萄糖-6-磷酸酶(G-6-Pase)的表达,采用Western blot法检测小鼠肝组织中腺苷酸活化蛋白激酶(AMPK)的表达。结果:与HFG组比较,TMP可显著降低T2DM小鼠体重和空腹血糖(P<0.01);TMP可使T2DM小鼠肝组织中PEPCK和G-6-Pase的m RNA和蛋白表达水平明显降低(P<0.01);TMP可显著提高T2DM小鼠肝组织中AMPK蛋白的磷酸化水平。结论:TMP可能通过促进肝脏AMPK的磷酸化,抑制PEPCK和G-6-Pase的表达,进而抑制肝脏糖异生,发挥抗T2DM的作用。 Objective: To explore the intervention effect of tricholoma matsutake polysaccharide(TMP)on type2 diabetes mellitus(T2DM)model in mice,and to clarify the mechanism of TMP anti-T2DM.Methods: The TMP was obtained by extracting the extract pine antler by ultrasonic-microwave synergistic extraction method.High-fat diet was adopted to induce and construct the mice T2DM model.T2DM mice were randomly divided into model group(HFG group),rosiglitazone positive control group(Rosi group),TMP low dose group(TMP1 group),and TMP high dose group(TMP2 group).Normal saline was given to HFG group,rosiglitazone was given to Rosi group,and TMP was given to TMP1 group and TMP2 group.The expression of phosphoenolpyruvate carboxykinase(PEPCK)and glucose-6-phosphatase(G-6-Pase)in mice liver tissue were detected by real-time fluorescence quantitative polymerase chain reaction(qPCR)and Western Blot,and the expression of adenylate activated protein kinase(AMPK)in mice liver tissue was detected by Western blot.Results: Compared with HFG group,TMP could significantly reduce the body weight and fasting blood-glucose of T2DM mice(P<0.01).TMP could significantly decrease the m RNA and protein expression of PEPCK and G-6-Pase in liver tissue of T2DM mice(P<0.01).TMP could significantly increase the phosphorylation level of AMPK protein in liver tissue of T2DM mice.Conclusion: TMP may play an anti-T2DM effect by promoting the phosphorylation of AMPK and inhibiting the expression of PEPCK and G-6-Pase,thus inhibiting gluconeogenesis in the liver.
作者 马婧 林箐 吴尤佳 房立平 Ma Jing;Lin Jing;Wu Youjia;Fang Liping(Zhangzhou Health Vocational College,Zhangzhou 363000,China;Peking University First Hospital,Peking 100034,China;Pharmaceutical College,Fujian Medical University,Fuzhou 350000,China)
出处 《广西医科大学学报》 CAS 2020年第4期705-709,共5页 Journal of Guangxi Medical University
基金 2017年福建省中青年教师教育教学科研课题资助项目(No.JAT171147)。
关键词 2型糖尿病 松茸多糖 糖异生 PEPCK G-6-pase AMPK type 2 diabetes mellitus tricholoma matsutake polysaccharide gluconeogenesis PEPCK G-6-pase AMPK
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