摘要
目的观察降糖宁胶囊(人参、山药、石膏、知母等)对Hep G2细胞糖代谢的影响,并探讨其降糖机制。方法体外培养人肝癌Hep G2细胞,MTT法检测降糖宁对细胞活力的影响;HE染色法观察降糖宁对细胞形态的影响;采用葡萄糖氧化酶法检测降糖宁对细胞糖消耗的影响;Western-blot检测磷酸化腺苷酸活化蛋白激酶(AMPK)及人胰岛素受体底物(IRS1)表达量。结果降糖宁胶囊对Hep G2细胞的活力和形态无明显影响,可明显促进Hep G2细胞对葡萄糖的消耗,能促进AMPKβ1/2、IRS1蛋白表达量。结论降糖宁胶囊的降糖机制可能涉及对胰岛素受体信号通路及AMPK信号通路的影响。
AIM To explore the effect of Jiangtangning Capsules( Ginseng Radix et Rhizoma,Dioscoreae Rhizoma,Gypsum Fibrosum,Anemarrhenae Rhizoma,etc.) on glucose metabolism of HepG2 cells in vitro and its mechanism.METHODS MTT assay was used to measure the viability of the HepG2 cells.HE staining was used for the observation of the morphological changes in HepG2 cells under the influence of Jiangtangning Capsules and glucose consumption was detected by oxidation enzyme method.The AMP-activated protein kinase( AMPK) and IRS-activated protein kinase( IRS1) were examined by Western-blot.RESULTS Jiangtangning Capsules could obviously promote the glucose consumption,AMPKβ1 /2,and the IRS1 protein expression of the HepG2 cells without affecting its viability or causing morphological change.CONCLUSION The hypoglycemic mechanism of Jiangtangning Capsules may be associated with insulin receptor signaling pathways and AMPK pathway.
引文
[1]李丽.中药治疗糖尿病的研究进展[J].河北医学,2013,19(5):762-764.
[2]陆怡,于建荣.国际糖尿病研发态势[J].生命科学,2012,24(7):634-639.
[3]李廷振,陈晓雯.中药治疗糖尿病周围神经病变研究概况[J].实用中医药杂志,2012,28(10):891-892.
[4]马立新,刘建平.中药治疗2型糖尿病随机对照试验效应指标把握度的调查研究[J].中国中西医结合杂志,2012,32(1):119-123.
[5]汪巧巧,宋菊敏,刘小美,等.调脂降糖中药复方在2型糖尿病基础研究中的运用[J].中成药,2012,34(2):329-331.
[6]兰跃文,张丽,姜红梅.降糖宁胶囊治疗2型糖尿病临床疗效观察[J].中国医药指南,2010,8(14):271-272.
[7]杨长江,杨文科.降糖宁胶囊降糖作用[J].陕西中医,2005,26(8):857-858.
[8]邓书鸿,宋丽,段小菊,等.黄芪提取物HPLC指纹图谱与抗疲劳作用的相关分析[J].中药材,2013,36(2):260-264.
[9]栾海艳,张建华,赵晓莲,等.桔梗总皂苷对2型糖尿病肝病大鼠糖脂代谢影响的研究[J].中成药,2013,35(6):1307-1309.
[10]Rosa L M,Manzoni C,Castiglioni S,et al.Lupin seedγ-conglutin lowers blood glucose in hyperglycaemic rats and increases glucose consumption of HepG2 cells[J].Br J Nutri,2012,107(1):67-73.
[11]Kaur L,Han K S,Bains K,et al.Indian culinary plants enhance glucose-induced insulin secretion and glucose consumption in INS-1β-cells and 3T3-L1 adipocytes[J].Food Chem,2011,129(3):1120-1125.
[12]Hitomi H,Mehta P K,Taniyama Y,et al.Vascular smooth muscle insulin resistance,but not hypertrophic signaling,is independent of angiotensinⅡ-induced IRS1 phosphorylation by JNK[J].Am J Physiol Cell Physiol,2011,301(6):C1415-C1422.
[13]Bose S K,Shrivastava S,Meyer K,et al.Hepatitis C virus activates the m TOR/S6K1 signaling pathway in inhibiting IRS1function for insulin resistance[J].J Virol,2012,86(11):6315-6322.
[14]Hardie D G,Ross F A,Hawley S A.AMPK:a nutrient and energy sensor that maintains energy homeostasis[J].Na Rev Mol Cell Biol,2012,13(4):251-262.
[15]Ruderman N B,Carling D,Prentki M,et al.AMPK,insulin resistance,and the metabolic syndrome[J].J Clin Inves,2013,123(7):2764-2772.
[16]Wrighton K H.Cell cycle:AMPK moonlights in mitosis[J].Na Rev Mole Cell Biol,2012,13(2):64-65.
[17]Traore S F,Bui Q A,Ruan K H.Type-II diabetes and herbal medicine[J].Am J Integr Med,2012,1(2):2-13.
[18]Kim H S,Kim M J,Kim E J,et al.Berberine-induced AMPK activation inhibits the metastatic potential of melanoma cells via reduction of ERK activity and COX-2 protein expression[J].Biochem Pharm,2012,83(3):385-394.
[19]Bartlett J D,Joo C H,Jeong T S,et al.Matched work high-intensity interval and continuous running induce similar increases in PGC-1αmRNA,AMPK,p38,and p53 phosphorylation in human skeletal muscle[J].J Applied Physiol,2012,112(7):1135-1143.