Abstract：
BACKGROUND: Diabetes Mellitus (DM) is a metabolic disorder characterized by persistent hyperglycemia and/or insulin resistance. If left uncontrolled, it can lead to a combination of cardiac and renal alterations known as cardiorenal syndrome. Additionally, oxidative stress and inflammation contribute to tissue damage, thereby reducing the life expectancy of individuals with diabetes.
OBJECTIVE: The aim of this study was to identify early molecular markers associated with cardiorenal syndrome, oxidative stress, and inflammation, and to investigate their correlation with the duration of exposure to DM.
METHODS: An experimental DM model was employed using Wistar rats. The rats were divided into four groups: diabetic rats at 7 days (DM7), diabetic rats at 30 days (DM30), control sham at 7 days (CS7), and control sham at 30 days (CS30). Blood and brain tissue from the brainstem region were collected at 7 and 30 days after confirming DM induction. Gene expression analysis of Bnp, Anp, Cat, Gpx, Sod, Tnf-α, and Il-6 was performed.
RESULTS: The analysis revealed lower expression values of Cat in the brainstem tissue of the DM7 group compared to the NDS7 group. Moreover, diabetic animals exhibited statistically lower levels of Tnf-α in their peripheral blood compared to the control animals.
CONCLUSIONS: This study concluded that DM alters the oxidative balance in the brainstem after 7 days of DM induction, resulting in lower Cat expression levels. Although some genes did not show statistical differences after 30 days of DM induction, other genes exhibited no expression values, indicating possible gene silencing. The study identified an imbalance in the studied pathways and concluded that the organism undergoes a compensatory state in response to the initial metabolic alterations caused by DM.
OBJECTIVE: The aim of this study was to identify early molecular markers associated with cardiorenal syndrome, oxidative stress, and inflammation, and to investigate their correlation with the duration of exposure to DM.
METHODS: An experimental DM model was employed using Wistar rats. The rats were divided into four groups: diabetic rats at 7 days (DM7), diabetic rats at 30 days (DM30), control sham at 7 days (CS7), and control sham at 30 days (CS30). Blood and brain tissue from the brainstem region were collected at 7 and 30 days after confirming DM induction. Gene expression analysis of Bnp, Anp, Cat, Gpx, Sod, Tnf-α, and Il-6 was performed.
RESULTS: The analysis revealed lower expression values of Cat in the brainstem tissue of the DM7 group compared to the NDS7 group. Moreover, diabetic animals exhibited statistically lower levels of Tnf-α in their peripheral blood compared to the control animals.
CONCLUSIONS: This study concluded that DM alters the oxidative balance in the brainstem after 7 days of DM induction, resulting in lower Cat expression levels. Although some genes did not show statistical differences after 30 days of DM induction, other genes exhibited no expression values, indicating possible gene silencing. The study identified an imbalance in the studied pathways and concluded that the organism undergoes a compensatory state in response to the initial metabolic alterations caused by DM.
摘要：
背景：糖尿病（DM）是一种以持续高血糖和/或胰岛素抵抗为特征的代谢紊乱。如果不受控制，它可以导致心脏和肾脏改变的组合，称为心肾综合征。此外,氧化应激和炎症导致组织损伤，从而降低糖尿病患者的预期寿命。
目的：本研究的目的是确定与心肾综合征相关的早期分子标志物，氧化应激，和炎症，并研究它们与DM暴露持续时间的相关性。
方法：采用Wistar大鼠建立实验性DM模型。将大鼠分为四组:糖尿病大鼠在7天(DM7),30天的糖尿病大鼠（DM30），7天对照假（CS7），和对照假在30天(CS30)。在确认DM诱导后7天和30天收集来自脑干区域的血液和脑组织。Bnp基因表达分析,Anp,猫,Gpx,Sod,Tnf-α,并进行了Il-6。
结果：分析显示，与NDS7组相比，DM7组脑干组织中Cat的表达值较低。此外，与对照动物相比,糖尿病动物外周血中Tnf-α的水平在统计学上较低.
结论：这项研究得出结论，DM诱导7天后，脑干中的氧化平衡发生了改变，导致较低的Cat表达水平。虽然一些基因在DM诱导30天后没有显示出统计学差异，其他基因没有表现出表达值，表明可能的基因沉默。该研究确定了所研究途径的不平衡，并得出结论，生物体响应于DM引起的初始代谢改变而处于补偿状态。
目的：本研究的目的是确定与心肾综合征相关的早期分子标志物，氧化应激，和炎症，并研究它们与DM暴露持续时间的相关性。
方法：采用Wistar大鼠建立实验性DM模型。将大鼠分为四组:糖尿病大鼠在7天(DM7),30天的糖尿病大鼠（DM30），7天对照假（CS7），和对照假在30天(CS30)。在确认DM诱导后7天和30天收集来自脑干区域的血液和脑组织。Bnp基因表达分析,Anp,猫,Gpx,Sod,Tnf-α,并进行了Il-6。
结果：分析显示，与NDS7组相比，DM7组脑干组织中Cat的表达值较低。此外，与对照动物相比,糖尿病动物外周血中Tnf-α的水平在统计学上较低.
结论：这项研究得出结论，DM诱导7天后，脑干中的氧化平衡发生了改变，导致较低的Cat表达水平。虽然一些基因在DM诱导30天后没有显示出统计学差异，其他基因没有表现出表达值，表明可能的基因沉默。该研究确定了所研究途径的不平衡，并得出结论，生物体响应于DM引起的初始代谢改变而处于补偿状态。
