摘要
该研究采用高糖高脂饮食结合小剂量链脲佐菌素（STZ）诱导的方法复制2型糖尿病（T2DM）大鼠模型。考察了给药后30 d各组动物胰岛素抵抗指数（HOMA-IR）及血清甘油三酯（TG）含量,并采用Western blot,RT-PCR法检测肝组织中固醇调节元件结合蛋白-1c（SREBP-1c）及其裂解激活蛋白（SCAP）表达情况,从而探讨中药黄连在改善T2DM机体胰岛素抵抗的同时,改善脂质代谢紊乱的分子机制。研究结果表明,2种黄连均能有效缓解机体胰岛素抵抗现象,降低血清TG含量,并下调肝组织SREBP-1c,SCAP的表达,其中,雅连组与模型组相比,相关蛋白及基因表达有显著性差异（P〈0.05,P〈0.01）。该结果提示,尽管雅连改善机体胰岛素抵抗作用不及味连,但降脂药效却优于味连;抑制SCAP/SREBP通路蛋白表达可能是中药黄连减少糖尿病机体脂质沉积的途径之一。
The type 2 diabetes rat model was induced with high-sugar and high-fat diet combined with low-dose STZ. This study investigated the hypolipidemic mechanism of Coptis chinensis and C. deltoidea. After 30 days of administration,HOMA-IR and the content of TG in serum were detected,and the expressions of SCAP,SREBP-1 c were tested by the method of Western blot and Real-time PCR analysis. The test results showed that both components can significantly alleviate insulin resistance and down-regulate the expressions of SREBP-1 c and SCAP in liver tissue of type two diabetes mellitus. Compared with the control group,there were significant differences in relevant protein expression（ P 〈 0. 05,P 〈 0. 01）. This indicates that the inhibition of SREBP-1 c and SCAP expressions may be the hypolipidemic mechanism of Coptidis Rhizoma on type 2 diabetes mellitus. The results also showed that C. deltoidea has a better efficacy in lipid elimination,but a weaker hypoglycemic effect against C. chinensis.
作者
刘睿颖
张思远
任彬
何雨蔓
顾健
谭睿
LIU Rui-ying;ZHANG Si-yuan;REN Bin;HE Yu-man;GU Jian;TAN Rui(College of Life Science and Engineering, Southwest Jaotong University, Chengdu 610031, China;School of Pharmacy, Southwest University for Nationalities, Chengdu 610051, China;Medical College, Southwest Jaotong University, Chengdu 610031, China)
出处
《中国中药杂志》
CAS
CSCD
北大核心
2018年第10期2129-2133,共5页
China Journal of Chinese Materia Medica
基金
国家自然科学基金青年基金项目(81703813)
四川省中医药管理局重点项目(2016Z008)
国家“重大新药创制”科技重大专项(2013ZX09103-002-014)
四川中医药资源普查成果转化项目(2016z014)
四川省中医药管理局2016科技项目(2016Q038)
四川省中医药管理局2017科技项目(2017C001)
关键词
味连
雅连
2型糖尿病
胰岛素抵抗
脂代谢
信号通路
Coptis chinensis
Coptis deltoidea
type 2 diabetes mellitus
insulin resistance
lipid metabolism
signal pathway
