Wistar大鼠实验性糖尿病发生及病程的分子机制研究

T. Ivanenko
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摘要

糖尿病的发生和发展涉及多种分子机制,特别是胰岛素抵抗、β细胞功能障碍、炎症过程。这些机制可以破坏胰岛素信号通路,促进β细胞凋亡,并且不一定依赖于细胞因子和趋化因子的干预。此外,基因也起着一定的作用,因为某些形式的糖尿病是由影响胰岛素产生或敏感性的基因突变引起的。糖尿病发生和发展的分子机制是复杂的,包含了人体生理和生物化学的各个方面。了解这些机制对于开发治疗和预防糖尿病的有效方法至关重要。这项工作的目的是分析Wistar大鼠胰腺组织样本中与糖尿病相关的基因表达。材料和方法。使用RTI Profiler™PCR阵列大鼠糖尿病试剂盒(QIAGEN, Germany),采用实时反转录聚合酶链反应方法分析基因表达,其中胰腺是实验动物的研究对象。RTI Profiler™PCR阵列大鼠糖尿病分析84个基因的表达,与糖尿病的发病、发展和进展相关。该基因组包含导致肥胖、胰岛素抵抗、早发性糖尿病及其晚期并发症的基因。这些基因由功能类别来表示:受体、转运体和通道;核受体;代谢酶;分泌的因素;信号转导蛋白;转录因子。根据对照组动物和实验性糖尿病动物的PCR研究结果,我们建立了Nkx2-1基因的活性;Pik3r1;与对照动物相比,Slc14a2具有高表达。与对照组相比,Nkx2-1基因的高表达活性证明其与糖尿病的发病机制有关。此外,Pik3r1蛋白在实验性糖尿病动物组中表达水平升高。这些变化被认为是一种代偿机制的一部分,旨在保持胰腺内分泌系统的细胞功能。此外,观察到的Slc14a2蛋白表达的增加可能表明糖尿病过程中与肾脏病理相关的晚期并发症的发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Determination of molecular mechanisms of development and course of experimental diabetes mellitus in Wistar rats
The development and progression of diabetes involves several molecular mechanisms, in particular: insulin resistance, dysfunction of beta cells, inflammatory processes. These mechanisms can disrupt insulin signaling pathways, contribute to beta-cell apoptosis, and are not necessarily dependent on the intervention of cytokines and chemokines. Additionally, genetics play a role, as some forms of diabetes are caused by genetic mutations affecting insulin production or sensitivity. The molecular mechanisms underlying the development and progression of diabetes are complex and encompass various aspects of the body’s physiology and biochemistry. Understanding these mechanisms is crucial for the development of effective methods for treating and preventing diabetes. The aim of the work is analysis of the expression of genes, related to diabetes in pancreatic tissue samples of Wistar rats. Materials and methods. The polymerase chain reaction method with real-time reverse transcription was used to analyze gene expression using the RTI Profiler™ PCR Array Rat Diabetes kit (QIAGEN, Germany), where the pancreas was the object of research in experimental animals. Results. RTI Profiler™ PCR Array Rat Diabetes profiles the expression of 84 genes, associated with the onset, development, and progression of diabetes. The panel contains genes that contribute to obesity, insulin resistance, early-onset diabetes, and its late complications. These genes are represented by functional categories: receptors, transporters, and channels; nuclear receptors; metabolic enzymes; secretion factors; signal transduction proteins; transcription factors. According to the PCR results of the study of the control group of animals and animals with experimental diabetes, we established the activity of the Nkx2-1 genes; Pik3r1; Slc14a2 with high expression compared to control animals. Conclusions. The Nkx2-1 gene has been implicated in the pathogenesis of diabetes, as evidenced by its high expression activity compared to the control group of animals. Additionally, the Pik3r1 protein shows elevated expression levels in the group of animals with experimental diabetes. These changes are believed to be part of a compensatory mechanism aimed at preserving the cellular function of the pancreatic endocrine system. Furthermore, the observed increase in Slc14a2 protein expression likely indicates the onset of late complications associated with kidney pathology in the course of diabetes.
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