盐知母降血糖活性部位对胰岛素抵抗作用的影响  被引量:8

Effects of the active fractions in salt processed Rhizoma Anemarrhenae on insulin resistance

在线阅读下载全文

作  者:张爽[1] 王晓婷[1] 高雁[1] 高慧[1] 

机构地区:[1]辽宁中医药大学药学院,辽宁大连116600

出  处:《中国医院药学杂志》2017年第21期2127-2130,共4页Chinese Journal of Hospital Pharmacy

基  金:国家自然科学基金(81102810);辽宁省自然科学基金(2013020165)

摘  要:目的:探讨盐知母降血糖活性部位对胰岛素抵抗作用的影响及其作用机制。方法:采用地塞米松诱导3T3-L1脂肪细胞胰岛素抵抗模型,比较盐知母降血糖活性部位对培养基中葡萄糖消耗的影响;采用STZ(链脲佐菌素)诱导大鼠胰岛素抵抗模型,给药14 d后测定大鼠空腹血糖值(FBG),并用试剂盒测定胰岛素、血浆瘦素、血浆抵抗素等水平。比较盐知母不同降血糖活性部位对2型糖尿病大鼠胰岛素抵抗作用的影响。结果:盐知母降血糖活性部位均能显著增加胰岛素抵抗3T3-L1脂肪细胞培养基中的葡萄糖消耗量,且盐知母三氯甲烷层萃取组作用最佳;与模型组相比,各给药组均显著改善糖尿病大鼠FBG、OGTT、Hb Alc、Homa-IR等水平及LEP、ADPN等胰岛素抵抗水平。结论:盐知母降血糖活性部位能够改善胰岛素抵抗作用,且三氯甲烷萃取层作用显著。OBJECTIVE To investigate the influences of the hypoglycemic active fractions in salt Rhizoma Anemarrhenae (SPAR) on insulin resistance,and its possible mechanism.METHODS The insulin resistant model was established by using dexamethasone with 3T3-L1 adipocyte cells to compare the effects of cellular glucose consumed by the different active fractions of the SPAR.Insulin resistant model was established by inducing rats with streptozotocin (STZ).Insulin,leptin and resistin were determined by using test kits,to compare the influences of the hypoglycemic active fractions in salt Rhizoma Anemarrhenae (SPAR) on insulin resistance.RESULTS The different active fractions of the SPAR could enhance cellular glucose consumed by insulin resistant adipocytes significantly,and the effect of the extractions of SPAR by chloroform was stronger.Compared with model control group,each treatment group obviously improved the blood glucose levels of FBG,OGTT,HbAlc,Homa-IR and the level of insulin resistance LEP,ADPN.CONCLUSION The hypoglycemic active fractions in SPAR can alleviate insulin resistance,and the effect of the extractions of SPAR by chloroform is obvious.

关 键 词:盐知母 活性部位 胰岛素抵抗 

分 类 号:R285.5[医药卫生—中药学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象