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目的研究胰岛素受体底物1(IRS-1)和胰岛素受体底物2(IRS-2)在宫内发育迟缓(IUGR)大鼠出生0周、3周和8周时肝脏组织中的表达,探讨IUGR个体易患代谢综合征(MS)的分子机制。方法采用母孕期低蛋白饮食法建立IUGR大鼠模型,应用反转录(RT)-PCR技术检测仔鼠在出生0周、3周、8周肝脏组织中IRS-1、IRS-2 mRNA水平,凝胶电泳条带用成像系统照相定量分析结果,分别计算PCR产物条带与β-actin条带吸光度值的比值,作为目的基因相对表达量。采用Western blot杂交检测仔鼠在出生0周、3周、8周肝脏组织IRS-1蛋白、IRS-2蛋白的水平表达。母孕期得到正常饮食的仔鼠作为对照组。结果 IUGR鼠出生时体质量显著低于对照组,出生后出现生长追赶,至8周时IUGR组体质量超过对照组;IUGR组0周、3周、8周时其肝脏组织IRS-2 mRNA和蛋白表达水平均显著低于对照组(Pa<0.05,0.01),肝脏组织IRS-1 mRNA和蛋白表达水平与对照组比较差异无统计学意义(Pa>0.05)。结论 IUGR大鼠0周、3周和8周肝脏组织中IRS-2 mRNA和蛋白水平显著下降,可能是IUGR个体易患MS的分子机制之一。
Objective To investigate the expression of insulin receptor substrate 1 (IRS-1) and insulin receptor substrate 2 (IRS-2) in liver tissues of IUGR rats at 0, 3 and 8 weeks after birth To investigate the molecular mechanism of IUGR susceptibility to metabolic syndrome (MS). Methods IUGR rat model was established by low protein diets during pregnancy and pregnancy. The levels of IRS-1 and IRS-2 mRNA in liver tissue of offspring were detected by RT-PCR at 0 week, 3 week and 8 week after birth. The gel electrophoresis bands were quantitatively analyzed with a photographic system of the imaging system to calculate the ratio of the absorbance value of the PCR product band and the β-actin band respectively as the relative expression level of the target gene. The levels of IRS-1 protein and IRS-2 protein in the liver of the offspring were detected by Western blot at 0, 3 and 8 weeks after birth. Pregnant mothers receive normal diet offspring as a control group. Results The body weight of IUGR mice was significantly lower than that of the control group at birth, and the growth of IUGR rats was chased after birth. The body weight of IUGR rats exceeded that of the control group by 8 weeks. The IRS-2 mRNA and protein expressions of IUGR group at 0 week, 3 weeks and 8 weeks (P <0.05, 0.01). The expression of IRS-1 mRNA and protein in liver tissue was not significantly different from the control group (Pa> 0.05). Conclusions IRS-2 mRNA and protein levels in liver tissue of IUGR rats at 0 week, 3 weeks and 8 weeks are significantly decreased, which may be one of the molecular mechanisms of IUGR susceptibility to MS.