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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Effects of Modified Sanzi Yangqin Decoction on Tyrosine Phosphorylation of IRS-1 in Skeletal Muscle of Type 2 Diabetic Rats
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Effects of Modified Sanzi Yangqin Decoction on Tyrosine Phosphorylation of IRS-1 in Skeletal Muscle of Type 2 Diabetic Rats

机译:加味三子养肾汤对2型糖尿病大鼠骨骼肌IRS-1酪氨酸磷酸化的影响

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This study aimed to investigate the effect of Modified Sanzi Yangqin Decoction on tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) in skeletal muscle of type 2 diabetic rats. The rat model of type 2 diabetes was induced by high-fat diet and multiple low-dose streptozotocin injections. Diabetic model rats were randomly divided into 5 groups the model control group, the metformin group, and Modified Sanzi Yangqin Decoction groups of low, medium, and high doses. OGTT was conducted every two weeks during treatment period. At the end of the treatment, the fasting blood glucose (FBG) level and the fasting C-peptide level were measured to calculate insulin resistance index. The levels of IRS-1, p-IRS-, and protein tyrosine phosphates 1B (PTP1B) in skeletal muscle were also measured. Modified Sanzi Yangqin Decoction significantly reduced the FBG level, increased the fasting C-peptide level, and lowered the insulin resistance index in type 2 diabetic rats. It also significantly increased the protein level of p-IRS- and reduced the PTP1B protein level in skeletal muscle of type 2 diabetic rats. Modified Sanzi Yangqin Decoction increases tyrosine phosphorylation of IRS-1 in skeletal muscle of type 2 diabetic rats, which results from the increase of p-IRS- protein and is related to the suppression of PTP1B protein.
机译:本研究旨在探讨加味三子养心汤对2型糖尿病大鼠骨骼肌胰岛素受体底物1(IRS-1)酪氨酸磷酸化的影响。高脂饮食和多次低剂量链脲佐菌素注射可诱发2型糖尿病大鼠模型。糖尿病模型大鼠随机分为低,中,高剂量模型对照组,二甲双胍组和加味三子养心汤组5组。在治疗期间每两周进行一次OGTT。在治疗结束时,测量空腹血糖(FBG)水平和空腹C肽水平以计算胰岛素抵抗指数。还测量了骨骼肌中IRS-1,p-IRS-和蛋白质酪氨酸磷酸酯1B(PTP1B)的水平。加味三子养心汤能明显降低2型糖尿病大鼠的FBG水平,提高空腹C肽水平和降低胰岛素抵抗指数。它还显着增加了2型糖尿病大鼠骨骼肌中p-IRS-的蛋白质水平,并降低了PTP1B蛋白质水平。改良的三子养心汤可增加2型糖尿病大鼠骨骼肌中IRS-1的酪氨酸磷酸化,这是由于p-IRS蛋白的增加所致,与PTP1B蛋白的抑制有关。

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