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.