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中国临床药理学与治疗学 ›› 2011, Vol. 16 ›› Issue (3): 263-269.

• 基础研究 • 上一篇    下一篇

黄芩苷对大鼠脂肪细胞胰岛素抵抗的改善作用

沈红燕, 吴晓冬   

  1. 东南大学医学院药理教研室,南京 210009,江苏
  • 收稿日期:2010-10-14 修回日期:2010-11-22 出版日期:2011-03-26 发布日期:2011-05-18
  • 通讯作者: 吴晓冬,男,博士,副教授,硕士生导师,研究方向:临床药理学。Tel: 13073489711 E-mail: roberwxd@yahoo.com.cn
  • 作者简介:沈红燕,女,硕士研究生,研究方向:临床药理学。Tel: 13584011065 E-mail: shynj123@163.com

Improvement effect of baicalin on dexamethasone-induced insulin resistance of rat adipocyte

SHEN Hong-yan , WU Xiao-dong   

  1. Department of Pharmacology, Medical School, Southeast University, Nanjing 210009, Jiangsu,China
  • Received:2010-10-14 Revised:2010-11-22 Online:2011-03-26 Published:2011-05-18

摘要: 目的: 探讨黄芩苷对大鼠脂肪细胞胰岛素抵抗的改善作用及可能机制。方法: 无菌条件下取大鼠腹股沟处的脂肪组织采用酶消化法进行原代培养,将前脂肪细胞诱导分化为成熟的脂肪细胞后,以地塞米松诱导建立胰岛素抵抗模型,待其抗性成立后予随机分组干预,分为4组:正常组、模型组、黄芩苷干预组和阳性药物(罗格列酮)干预组。以葡萄糖氧化酶法检测各组细胞上清液中的葡萄糖浓度,ELISA方法检测上清液中细胞因子脂连素(adiponectin)、抵抗素(resistin)的浓度,免疫组化法检测PPARγ的表达。结果: 黄芩苷干预组、阳性药物(罗格列酮)组与模型组相比能明显增加脂肪细胞葡萄糖消耗量(P<0.01),升高脂连素的水平(P<0.05, P<0.01)、降低抵抗素水平(P<0.05),PPARγ的表达增加(P<0.05,P<0.01)。结论: 黄芩苷能增加胰岛素抵抗脂肪细胞的葡萄糖消耗,改善胰岛素抵抗,其机制可能是通过上调PPARγ的表达升高脂连素水平并降低抵抗素水平。

关键词: 黄芩苷, 胰岛素抵抗, 脂连素, 抵抗素, 过氧化物酶体增殖物激活受体γ

Abstract: AIM: To study the improvement effect of baicalin on rat adipocyte insulin resistance and its mechanism.METHODS: Using enzyme-digesting method, proadipocyte cells from the rat inguinal adipose tissues which were cut under sterile conditions were cultured.The proadipocytes were induced to differentiate into mature adipocyte .Then adipocyte insulin resistance was induced by dexamethasone . Two groups of dexamethasone -induced insulin resistance adipocytes were given the following treatments for 48 hours: baicalin treated group(baicalin 20 μg/mL 48 h) ,rosiglitazone treated group(rosiglitazone 10 μmol/L 48 h) . In addition, vehicle-treated adipocytes and normal controls were used in the experiment. Glucose in every group adipocyte supernatant were detected by glucose oxidase. Enzyme-linked immunosorbent assay (ELISA) was employed to monitor the levels of supernatant adiponectin and resistin. The expression of PPARγ were detected by immumohisto-chemical technique.RESULTS: The levels of glucose consumption in baicalin treated group and rosiglitazone treated group were significantly increased compared with insulin resistance group (P<0.01). The levels of adiponectin and the expression of PPARγ were also increased in baicalin treated group and rosiglitazone treated group compared with insulin resistance group while the levels of resistin were decreased(P<0.05,P<0.01).CONCLUSION: Baicalin can increase glucose consumption in insulin resistance adipocyte and improve insulin resistance. The effect may be due to the increase of adiponectin induced by the upregulation of the expression of the PPARγand decrease of resistin.

Key words: Baicalin, Insulin resistance, Adiponectin, Resistin, PPARγ

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