Dexmedetomidine Alleviates Myocardial Injury Induced by Acute Kidney Injury in Diabetes Mellitus Rats via Regulating the Inflammatory Response.

IF 1.1 4区医学 Q4 MEDICAL LABORATORY TECHNOLOGY

Annals of clinical and laboratory science Pub Date : 2024-07-01

Qiang Geng, Yiheshan Ainiwaer, Jingjing Zhang, Bing Zhang

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引用次数: 0

Abstract

Objective: To study the effect of dexmedetomidine (Dex) on myocardial injury induced by acute kidney injury (AKI) in diabetes mellitus rats and explore the potential mechanisms.

Methods: The Type 2 diabetes mellitus (T2DM) model was prepared in 40 adult male Wistar rats. These rats were randomly divided into four groups (n=10/group), including the control (Con) group, AKI group, Dex preconditioning (DPreC) group, and resveratrol (Res) combined with Dex preconditioning (Res+DPreC) group. The AKI model was prepared in the AKI, DPreC, and Res+DPreC group. The DPreC group received Dex, while the Con and AKI group received normal saline. The Res+DPreC group received Res in addition to Dex preconditioning. Histopathologic, apoptotic, enzymatic, and inflammatory changes in myocardial tissue were observed or detected.

Results: Histopathologic, apoptotic, and enzymatic changes in myocardial tissue demonstrated that AKI induced myocardial injury in T2DM rats; Dex preconditioning could mitigate this injury; and RES enhanced this effect. Inflammatory changes suggested that Dex alleviated the inflammatory response induced by AKI in T2DM rats via regulating the expressions of SIRT1, TNF-α, IL-17A, and IL-10.

Conclusions: Dex could alleviate myocardial injury induced by AKI in DM rats via regulating the inflammatory response associated with SIRT1, TNF-α, IL-17A, and IL-10, and Res could enhance this protective effect.

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右美托咪定通过调节炎症反应减轻糖尿病大鼠急性肾损伤引起的心肌损伤

目的研究右美托咪定（Dex）对糖尿病大鼠急性肾损伤（AKI）所致心肌损伤的影响，并探讨其潜在机制：方法：用 40 只成年雄性 Wistar 大鼠制备 2 型糖尿病（T2DM）模型。这些大鼠被随机分为四组（n=10/组），包括对照（Con）组、AKI组、Dex预处理（DPreC）组和白藜芦醇（Res）联合Dex预处理（Res+DPreC）组。AKI组、DPreC组和Res+DPreC组准备了AKI模型。DPreC 组接受 Dex，而 Con 和 AKI 组接受生理盐水。Res+DPreC组在接受Dex预处理的同时还接受Res预处理。观察或检测心肌组织的组织病理学、凋亡、酶学和炎症变化：结果：心肌组织的组织病理学、凋亡和酶学变化表明，AKI 会诱发 T2DM 大鼠心肌损伤；Dex 预处理可减轻这种损伤；RES 可增强这种效果。炎症变化表明，Dex通过调节SIRT1、TNF-α、IL-17A和IL-10的表达，减轻了T2DM大鼠AKI诱导的炎症反应：结论：Dex可通过调节与SIRT1、TNF-α、IL-17A和IL-10相关的炎症反应减轻DM大鼠AKI引起的心肌损伤，Res可增强这种保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Annals of clinical and laboratory science 医学-医学实验技术

CiteScore

1.60

自引率

0.00%

发文量

112

审稿时长

6-12 weeks

期刊介绍： The Annals of Clinical & Laboratory Science welcomes manuscripts that report research in clinical science, including pathology, clinical chemistry, biotechnology, molecular biology, cytogenetics, microbiology, immunology, hematology, transfusion medicine, organ and tissue transplantation, therapeutics, toxicology, and clinical informatics.