Duan Bailu, Zhao Zhongqiu, Lin Ling, Jin Jing, Zhang Lijun, Xiong Hui, Ta Na, Gao Tiexiang, Mei Zhinan
College of Basic Medicine, Hubei University of Chinese Medicine, Wuhan 430065, China.
College of Pharmaceutical Sciences, South-Central University for Nationalities, Wuhan 430074, China.
Evid Based Complement Alternat Med. 2017;2017:7302965. doi: 10.1155/2017/7302965. Epub 2017 Aug 17.
The aim of this study was to investigate the antidiabetic effects of a Tibetan medicine, Tang-Kang-Fu-San (TKFS), on experimental type 2 diabetes mellitus (T2DM) rats and to explore its underlying mechanisms. Firstly two major chemical compositions of TKFS, gallic acid and curcumin, were characterized by HPLC fingerprint analysis. Next T2DM in rats was induced by high-fat diet and a low-dose streptozotocin (STZ 35 mg/kg). Then oral gavage administration of three different doses of TKFS (0.3 g/kg, 0.6 g/kg, and 1.2 g/kg) was given to T2DM rats. Experimental results showed that TKFS dramatically reduced the levels of fasting blood glucose, fasting blood insulin, triglyceride, total cholesterol, LDL cholesterol, and HDL cholesterol, even though it did not alter the animal body weight. The downregulation of phosphorylation-AKT (p-AKT) and glucose transporter-4 (GLUT4) in skeletal muscle of T2DM rats was restored and abnormal pathological changes in pancreas tissues were also improved. Our work showed that TKFS could alleviate diabetic syndromes, maintain the glucose homeostasis, and protect against insulin resistance in T2DM rats, and the improvement of AKT phosphorylation and GLUT4 translocation in skeletal muscle would be one of its possible underlying mechanisms.
本研究旨在探讨藏药糖康福散（TKFS）对实验性2型糖尿病（T2DM）大鼠的抗糖尿病作用，并探究其潜在机制。首先，通过高效液相色谱指纹图谱分析对TKFS的两种主要化学成分没食子酸和姜黄素进行了表征。接下来，采用高脂饮食和低剂量链脲佐菌素（STZ 35mg/kg）诱导大鼠发生T2DM。然后，对T2DM大鼠进行三种不同剂量TKFS（0.3g/kg、0.6g/kg和1.2g/kg）的灌胃给药。实验结果表明，TKFS显著降低了空腹血糖、空腹血胰岛素、甘油三酯、总胆固醇、低密度脂蛋白胆固醇和高密度脂蛋白胆固醇水平，尽管它并未改变动物体重。T2DM大鼠骨骼肌中磷酸化-AKT（p-AKT）和葡萄糖转运蛋白4（GLUT4）的下调得以恢复，胰腺组织的异常病理变化也得到改善。我们的研究表明，TKFS可以缓解糖尿病症状，维持血糖稳态，并预防T2DM大鼠的胰岛素抵抗，骨骼肌中AKT磷酸化和GLUT4易位的改善可能是其潜在机制之一。
