Qiu Guizhen, Tian Wei, Huan Mei, Chen Jinlong, Fu Haitao
1 Department of Health, Linyi People's Hospital of Shandong University, Linyi 276003, Shandong Province, China.
2 Department of Nursing, Linyi Oncosurgical Hospital, Linyi 276002, Shandong Province, China.
Exp Biol Med (Maywood). 2017 Jan;242(2):223-230. doi: 10.1177/1535370216657445. Epub 2016 Jul 24.
The aim of this study was to investigate the anti-hyperglycemic activity and mechanism of formononetin in alloxan-induced type 1 diabetic mice by determining its effect on some diabetes-related indices as described below. Body weight, fasting blood glucose, hepatic glycogen, serum insulin, and serum glucagon were determined by electronic scales, glucometer, and ELISA kits. Fas, Caspase-3, pancreatic and duodenal homeobox-1 , insulin receptor substrate 2, glucokinase and glucose transporter 2, mRNA and proteins levels in pancreas tissue, and glucokinase and glucose-6-phosphatase mRNA, and proteins levels in liver tissue were detected by fluorogenic quantitative-polymerase chain reaction and Western blot assays. The results indicated that formononetin (5, 10, and 20 mg/kg; oral administration) reversed the alloxan-induced increase of some indices (fasting blood glucose level and Fas and Caspase-3 mRNA and proteins levels in pancreas tissue) and reduction of some indices (body weight gain, oral glucose tolerance, insulin activity, hepatic glycogen level, pancreatic and duodenal homeobox-1, insulin receptor substrate 2, glucokinase and glucose transporter 2, mRNA and proteins levels in pancreas tissue, and glucokinase mRNA and protein levels in liver tissue). The glucagon level and glucose-6-phosphatase mRNA and protein levels in liver tissue were not affected by the drugs administration. In conclusion, formononetin exhibited anti-hyperglycemic activity in alloxan-induced type 1 diabetic mice by inhibiting islet B cell apoptosis and promoting islet B cell regeneration, insulin secretion, hepatic glycogen synthesis, and hepatic glycolysis.
本研究的目的是通过测定其对以下所述的一些糖尿病相关指标的影响，来研究芒柄花黄素在四氧嘧啶诱导的1型糖尿病小鼠中的降血糖活性及机制。体重、空腹血糖、肝糖原、血清胰岛素和血清胰高血糖素通过电子秤、血糖仪和ELISA试剂盒进行测定。通过荧光定量聚合酶链反应和蛋白质免疫印迹法检测胰腺组织中Fas、半胱天冬酶 - 3、胰腺十二指肠同源盒 - 1、胰岛素受体底物2、葡萄糖激酶和葡萄糖转运蛋白2的mRNA和蛋白质水平，以及肝组织中葡萄糖激酶和葡萄糖 - 6 - 磷酸酶的mRNA和蛋白质水平。结果表明，芒柄花黄素（5、10和20mg/kg；口服给药）可逆转四氧嘧啶诱导的一些指标升高（空腹血糖水平以及胰腺组织中Fas和半胱天冬酶 - 3的mRNA和蛋白质水平），并逆转一些指标降低（体重增加、口服葡萄糖耐量、胰岛素活性、肝糖原水平、胰腺十二指肠同源盒 - 1、胰岛素受体底物2、葡萄糖激酶和葡萄糖转运蛋白2在胰腺组织中的mRNA和蛋白质水平，以及肝组织中葡萄糖激酶的mRNA和蛋白质水平）。肝组织中的胰高血糖素水平以及葡萄糖 - 6 - 磷酸酶的mRNA和蛋白质水平不受药物给药的影响。总之，芒柄花黄素通过抑制胰岛B细胞凋亡并促进胰岛B细胞再生、胰岛素分泌、肝糖原合成和肝糖酵解，在四氧嘧啶诱导的1型糖尿病小鼠中表现出降血糖活性。
