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.

Dexmedetomidine Attenuates Myocardial Injury Induced by Renal Ischemia/Reperfusion by Inhibiting the HMGB1-TLR4-MyD88-NF-κB Signaling Pathway.

Objective: To investigate the effect of dexmedetomidine (DEX) on myocardial injury induced by renal ischemia/reperfusion (I/R) and to explore the role of the HMGB1-TLR4-MyD88-NF-κB signaling pathway.

Methods: Adult male Wistar rats were randomly allocated into the control group, renal I/R group, renal I/R group pretreated with a low dose of DEX (L-Dex+I/R), renal I/R group pretreated with a medium dose of DEX (M-Dex+I/R), and renal I/R group pretreated with a high dose of DEX (H-Dex+I/R). Outcome measures included the plasma concentrations of HMGB1, IL-6, IL-10, IL-17, and TnI, the expression levels of HMGB1, TLR4, MyD88, NF-κBp65, and P-NF-κBp65, the pathological change, and the cell apoptosis.