Seo Yun-Soo, Shon Mi-Yae, Kong Ryong, Kang Ok-Hwa, Zhou Tian, Kim Do-Yeon, Kwon Dong-Yeul
Department of Oriental Pharmacy, College of Pharmacy and Wonkwang-Oriental Medicines Research Institute, Wonkwang University, Iksan, Jeonbuk 570-749, Republic of Korea.
International Ginseng and Herb Research Institute, Geumsan, 312-804, Republic of Korea.
J Ethnopharmacol. 2016 Aug 22;190:231-40. doi: 10.1016/j.jep.2016.05.060. Epub 2016 May 31.
Ginseng (Panax ginseng C. A. Meyer, Araliaceae) has been used as a traditional medicine for thousands of years for the treatment of a wide variety of diseases, including diabetes. Processed ginseng named Black ginseng exhibits more potent biological activities than white and red ginseng. The aim of this study was to investigate the effects of black ginseng extract (GBG05-FF) on hyperglycemia and glucose tolerance in streptozotocin (STZ)-induced diabetic mice.
Black ginseng was produced by a repeated steaming and drying process, subsequent extraction with 70% ethanol, filtration, and lyophilization. The effect of GBG05-FF on glucose uptake and related protein expression and phosphorylation were determined in C2C12 cells. Furthermore, we evaluated the anti-diabetic effects of GBG05-FF in STZ-induced diabetic mice.
GBG05-FF significantly (p<0.05) increased glucose uptake in C2C12 myotubes via AMPK, Sirt1 and PI3-K pathway. In addition, GBG05-FF improved the fasting blood glucose levels and glucose tolerance in STZ-induced diabetic mice. GBG05-FF decreased blood parameters such as glycated hemoglobin, triglyceride and total cholesterol. Quantitative RT-PCR assay revealed that in the STZ-induced diabetic mice treated with GBG05-FF, the expression of hepatic genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase (PEPCK), glucose 6-phosphatase (G6Pase)), glycogenolysis (liver glycogen phosphorylase (LGP)) and glycogenesis (glycogen synthase (GS)) was suppressed, while the expression of the genes involved in glucose uptake (glucose transporter (GLUT) 1, GLUT4) and β-oxidation (acyl-CoA oxidase (ACO), carnitine palmitoyl transferase 1a (CPT1a), mitochondrial medium chain acyl-CoA dehydrogenase (MCAD)) in muscle were increased. GBG05-FF delayed diabetes-associated muscle atrophy by activating mTOR. The major bioactive compounds including ginsenoside Rg1, Rg3(S), Rg3(R), Rg5, Rk1 and Rh4 were evaluated for glucose uptake effect in C2C12 myotubes; the data indicated that Rh4 significantly (p<0.05) increased glucose uptake.
Collectively, the results suggested that GBG05-FF is a potentially useful agent for treatment of diabetes by increasing glucose uptake.
人参（五加科人参属的人参C.A.迈耶）作为一种传统药物已被使用了数千年，用于治疗包括糖尿病在内的多种疾病。名为黑参的加工人参比白参和红参具有更强的生物活性。本研究的目的是研究黑参提取物（GBG05-FF）对链脲佐菌素（STZ）诱导的糖尿病小鼠高血糖和葡萄糖耐量的影响。
通过反复蒸煮干燥过程制备黑参，随后用70%乙醇提取、过滤并冻干。在C2C12细胞中测定GBG05-FF对葡萄糖摄取以及相关蛋白表达和磷酸化的影响。此外，我们评估了GBG05-FF对STZ诱导的糖尿病小鼠的抗糖尿病作用。
GBG05-FF通过AMPK、Sirt1和PI3-K途径显著（p<0.05）增加C2C12肌管中的葡萄糖摄取。此外，GBG05-FF改善了STZ诱导的糖尿病小鼠的空腹血糖水平和葡萄糖耐量。GBG05-FF降低了糖化血红蛋白、甘油三酯和总胆固醇等血液参数。定量RT-PCR分析显示，在用GBG05-FF治疗的STZ诱导的糖尿病小鼠中，参与糖异生（磷酸烯醇丙酮酸羧激酶（PEPCK）、葡萄糖6-磷酸酶（G6Pase））、糖原分解（肝糖原磷酸化酶（LGP））和糖原合成（糖原合酶（GS））的肝脏基因表达受到抑制，而参与肌肉中葡萄糖摄取（葡萄糖转运蛋白（GLUT）1、GLUT4）和β-氧化（酰基辅酶A氧化酶（ACO）、肉碱棕榈酰转移酶1a（CPT1a）、线粒体中链酰基辅酶A脱氢酶（MCAD））的基因表达增加。GBG05-FF通过激活mTOR延缓糖尿病相关的肌肉萎缩。评估了包括人参皂苷Rg1、Rg3(S)、Rg3(R)、Rg5、Rk1和Rh4在内的主要生物活性化合物对C2C12肌管葡萄糖摄取的影响；数据表明Rh4显著（p<0.05）增加葡萄糖摄取。
总体而言，结果表明GBG05-FF可能是一种通过增加葡萄糖摄取来治疗糖尿病的有用药物。
