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引用次数: 0
摘要
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。
Dexmedetomidine Alleviates Myocardial Injury Induced by Acute Kidney Injury in Diabetes Mellitus Rats via Regulating the Inflammatory Response.
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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