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作 者:张毅[1] 赵丹丹[2] 莫芳芳[2] 高思华[2] ZHANG Yi;ZHAO Dandan;MO Fangfang;GAO Sihua(Beijing Open University,Beijing 100081,China;Beijing University of Chinese Medicine,Beijing 100029,China)
机构地区:[1]北京开放大学,北京100081 [2]北京中医药大学,北京100029
出 处:《天津中医药》2022年第1期90-95,共6页Tianjin Journal of Traditional Chinese Medicine
基 金:国家中医药领军人才支持计划——岐黄学者(10400633210005);国家自然科学基金项目(NSFC81503540);重大新药创制子课题(2012ZX09103201-005)。
摘 要:[目的]通过检测2型糖尿病小鼠肝糖原含量及相关指标的变化,探讨降糖消渴颗粒对糖尿病状态下肝糖原合成及储备的影响。[方法]选取雄性8周龄KK-Ay小鼠,予以高脂饲料喂养,诱导建立2型糖尿病模型,以空腹血糖≥13.9 mmol/L为成模标准;C57BL/6J小鼠予以正常饲料喂养,作为对照组。将成模后小鼠随机分为模型组、吡格列酮组、降糖消渴颗粒低、中、高(1.75、3.50、7.00 g/kg)剂量组,口服给药10周后,计算各组小鼠日均进食量及体质量增长率的变化;过碘酸雪夫染色法检测小鼠肝脏中糖原含量的变化;逆转录-聚合酶链式反应(RT-PCR)法检测小鼠肝脏IRS-2 mRNA、Akt mRNA、GSK-3αmRNA的表达情况。[结果]中剂量(3.50 g/kg)降糖消渴颗粒可显著提高肝组织中IRS-2 mRNA、Akt mRNA,降低GSK-3αmRNA的表达(P<0.01),增加肝脏中糖原的储备量(P<0.05);高剂量(7.00 g/kg)也具有提高肝组织中IRS-2 mRNA,降低GSK-3αmRNA表达(P<0.01)的作用。[结论]降糖消渴颗粒可增加糖尿病小鼠肝脏胰岛素受体与糖代谢相关基因的表达,从而促进肝脏利用血糖合成糖原,增加肝脏糖原储备,改善糖尿病糖代谢紊乱状态。[Objective]To investigate the effect of Jiangtang Xiaoke Granule(JTXKG)on liver glycogen content andhepatic insulin receptor substrate-2(IRS-2)mRNA,protein kinase B,PKB/Akt(Akt)mRNA,glycogen synthase kinase 3α(GSK-3α)mRNA expression in type 2 diabetic KK-Ay mice.[Methods]KK-Ay mice,male,8 weeks old,were fed by high-fat-diet for 4 weeks,T2DM model were established by FBG≥13.9 mmol/L.The T2DM mice were then randomly divided into model group,pioglitazone group and JTXKG groups in low(1.75 g/kg),medium(3.50 g/kg),and high(7.00 g/kg)doses.The normal group had C57BL/6J in it and feed by normal diet.After 10-week treatment,the average daily food intake and the rate of weight gain were weighed and calculated.The liver glycogen was examined by Periodic Acid-Schiff stain.The expressions of GSK-3αwas examined by real-time fluorescence quantitative PCR,and the effects of JTXKG on the above indexes were observed.[Results]Compared with model group,T2DM mice supplemented with 3.50 g/kg dose of JTXKG can lower GSK-3αmRNA expression(P<0.01)and raise IRS-2 mRNA(P<0.01),Akt mRNA(P<0.01)expression to restore more liver glycogen(P<0.05).The 7 g/kg dose of JTXKG also can raise IRS-2 mRNA and lower hepatic GSK-3αmRNA expression of T2DM mice significantly(P<0.01).[Conclusion]JTXKG can raised the liver glycogen synthetize and repertory function in T2DM mice by regulating hepatic glycometabolism related gene expressions.
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