| 引用本文: | 邱士玉,康白,王志新,张广学,张秀荣,李承德.二甲双胍改善去势大鼠胰岛素抵抗的机制研究[J].中国现代应用药学,2013,30(3):243-245. |
| QIU Shiyu,,KANG Bai ,WANG Zhixin,ZHANG Guangxue,ZHANG Xiurong,LI Chengde.Metformin Mechanism of Insulin Resistance in Ovariectormized Female Rats[J].Chin J Mod Appl Pharm(中国现代应用药学),2013,30(3):243-245. |
|
| 摘要: |
| 目的 探讨二甲双胍(MF)对去势雌性大鼠胰岛素抵抗的改善作用及机制。方法 采用放射免疫分析法RIA测定血清雌二醇(E2)、孕酮(P)、胰岛素(INS)的水平，采用酶联免疫吸附试验ELISA测定肿瘤坏死因子-α(TNF-α)的水平，采用逆转录聚合酶链反应RT-PCR测定胰岛细胞因子信号转导抑制因子-3(suppressor of cytokine sighting-3，SOCS-3)的基因表达。结果 与假手术(SHAM)组比较，去势(OVX)模型组E2、P的含量显著降低，而TNF-α、INS含量则明显升高，同时大鼠胰岛SOCS-3基因表达明显上调(P<0.01)。与OVX组比较，去势二甲双胍低剂量(MF低)组无显著影响，去势二甲双胍高剂量(MF高)组E2、P含量则显著升高(P<0.05)，INS含量明显降低(P<0.05或P<0.01)，大鼠胰岛SOCS-3基因表达明显下调(P<0.01)。结论 长期大剂量使用MF可以改善去势大鼠的胰岛素抵抗现象，其机制可能与下调TNF-α和胰岛SOCS-3基因表达有关。 |
| 关键词: 二甲双胍 胰岛素抵抗 肿瘤坏死因子-α 细胞因子信号转导抑制因子-3 |
| DOI： |
| 分类号: |
| 基金项目: |
|
| Metformin Mechanism of Insulin Resistance in Ovariectormized Female Rats |
|
QIU Shiyu,, KANG Bai , WANG Zhixin, ZHANG Guangxue, ZHANG Xiurong, LI Chengde
|
|
Pharmacology Laboratory of Weifang Medical College, Weifang 261053, China
|
| Abstract: |
| OBJECTIVE To investigate the improvement effect and mechanism of metformin(MF) on insulin resistance in castrated female rats. METHODS The levels of serum estradiol(E2), progesterone (P) and insulin (INS) were determined by radioimmunoassay method. Tumor necrosis factor-a (TNF-α) level was measured by enzyme-linked immunosorbent assay. Gene expression of pancreas islet suppressor of cytokine sighting-3(SOCS-3) was determined by using reverse transcriptase polymerase chain reaction. RESULTS Compared with NS group, the serum E2 and P content in OVX group were significantly decreased, the TNF-α, INS content were significantly increased , while the SOCS-3 mRNA expression of pancreas islets were significantly increased(P<0.01). Compared with the OVX group, MF low group has no significant change. Serum E2 and P content were significantly increased (P<0.05) in MF high group. The TNF-α, INS content significantly decreased (P<0.05 or P<0.01), while the SOCS-3 mRNA expression of islets were significantly decreased (P<0.01). CONCLUSION Long-term with a large dose of MF 270 mg·kg-1·d-1can improve ovariectormized rats insulin resistance phenomenon. The mechanism may be related with the decreased of TNF-α and SOCS-3 mRNA expression of islets. |
| Key words: metformin insulin resistance TNF-α SOCS-3 |
