Bao Qinwen, Shen Xiaozhu, Qian Li, Gong Chen, Nie Maoxiao, Dong Yan
Department of Geriatric, Lianyungang Second People's Hospital of Jiangsu Province East Hospital, Jiangsu Province, Lianyungang 222002, PR China.
Department of Clinical, Lianyungang Second People's Hospital of Jiangsu Province East Hospital, Jiangsu Province, Lianyungang 222002, PR China.
Korean J Physiol Pharmacol. 2016 Mar;20(2):153-60. doi: 10.4196/kjpp.2016.20.2.153. Epub 2016 Feb 23.
The objective was to investigate the hypoglycemic action of catalpol in spontaneous diabetes db/db mice. 40 db/db mice were randomly divided into fi ve groups: model control gourp; db/db plus catalpol 40, 80, 120 mg/kg body wt. groups and db/db plus metformin 250 mg/kg group. Age-matched db/m mice were selected as normal control group. The mice were administered with corresponding drugs or solvent by gavage for 4 weeks. The oral glucose tolerance test was carried out at the end of 3(rd) week. After 4 weeks of treatment, the concentrations of fasting blood glucose (FBG), glycated serum protein (GSP), insulin (INS), triglyceride (TG), total cholesterol (TC) and adiponection (APN) in serum were detected. The protein expressions of phosphorylation-AMPKα1/2 in liver, phosphorylation-AMPKα1/2 and glucose transporter-4 (GLUT-4) in skeletal muscle and adipose tissues were detected by western blot. Real time RT-PCR was used to detect the mRNA expressions of acetyl-CoA carboxylase (ACC) and Hydroxymethyl glutaric acid acyl CoA reductase (HMGCR) in liver. Our results showed that catalpol could significantly improve the insulin resistance, decrease the serum concentrations of INS, GSP, TG, and TC. The concentrations of APN in serum, the protein expression of phosphorylation-AMPKα1/2 in liver, phosphorylation-AMPKα1/2 and GLUT-4 in peripheral tissue were increased. Catalpol could also down regulate the mRNA expressions of ACC and HMGCR in liver. In conclusion, catalpol ameliorates diabetes in db/db mice. It has benefi t eff ects against lipid/glucose metabolism disorder and insulin resistance. The mechanism may be related to up-regulating the expression of phosphorylation-AMPKα1/2.
目的是研究梓醇对自发性糖尿病db/db小鼠的降血糖作用。将40只db/db小鼠随机分为五组：模型对照组；db/db加梓醇40、80、120mg/kg体重组和db/db加二甲双胍250mg/kg组。选择年龄匹配的db/m小鼠作为正常对照组。通过灌胃给予小鼠相应药物或溶剂，持续4周。在第3周结束时进行口服葡萄糖耐量试验。治疗4周后，检测血清中空腹血糖（FBG）、糖化血清蛋白（GSP）、胰岛素（INS）、甘油三酯（TG）、总胆固醇（TC）和脂联素（APN）的浓度。通过蛋白质免疫印迹法检测肝脏中磷酸化-AMPKα1/2、骨骼肌和脂肪组织中磷酸化-AMPKα1/2和葡萄糖转运蛋白-4（GLUT-4）的蛋白表达。采用实时逆转录-聚合酶链反应检测肝脏中乙酰辅酶A羧化酶（ACC）和羟甲基戊二酸单酰辅酶A还原酶（HMGCR）的mRNA表达。我们的结果表明，梓醇可显著改善胰岛素抵抗，降低血清中INS、GSP、TG和TC的浓度。血清中APN的浓度、肝脏中磷酸化-AMPKα1/2的蛋白表达、外周组织中磷酸化-AMPKα1/2和GLUT-4的蛋白表达均增加。梓醇还可下调肝脏中ACC和HMGCR的mRNA表达。总之，梓醇可改善db/db小鼠的糖尿病症状。它对脂质/葡萄糖代谢紊乱和胰岛素抵抗具有有益作用。其机制可能与上调磷酸化-AMPKα1/2的表达有关。
