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Dexmedetomidine improves DM-induced oxidative stress injury to protect liver function through Nrf2 pathway
Lin Zeng1,2, Chunwu Zhao3,4, Chang Cui2,4
1Department of Anesthesiology, Shifang People's Hospital Deyang 618400, Sichuan, China.
Objective:
Diabetes mellitus-induced oxidative stress (OS) causes liver injury. Intraoperative pumping of dexmedetomidine (DEX) effectively reduced the postoperative OS response in patients with type 2 diabetes mellitus (T2DM) and had a certain protective effect on liver function. However, the mechanisms of the protective effect on the liver remained unclear. In this study, we investigated the antagonistic effects and the possible mechanism of DEX on T2DM-induced liver injury in the mouse model and Palmitic acid (Pal)-induced injury in hepatocellular carcinoma cells (HepG2).
Methods:
Seven wt/wt mice served as Control group, and 28 db/db mice were randomly divided into four groups using a random number table method: Model group (n=7), D25 group (n=7), D50 group (n=7) and D75 group (n=7). Different concentrations of DEX were injected intraperitoneally in the D25 group, D50 group and D75 group, while the Control group and the Model group were intraperitoneally injected with the same amount of normal saline for 3 weeks. In the cell intervention experiments, HepG2 cell line was used. The control group (Con group), the palmitic acid group (Pal group) and the DEX treatment group (Pal + Dex group) were set up. The test results were compared among mice groups and cell groups, respectively.
Results:
DEX alleviated the increase of alanine aminotransferase, triglyceride, total cholesterol and aspartate aminotransferase contents induced by high fat or T2DM. DEX reversed the decrease of nuclear factor E2 related factor 2 (Nrf2) in the nuclear translocation and the lower transcriptional activity of Nrf2 to inhibit the expression of heme oxygenase-1, NADPH quinone oxidoreductase-1 and superoxide dismutase 2 and reduced the activity of superoxide dismutase to increase reactive oxygen species content induced by high fat or T2DM.
Conclusion:
By attenuating the high-fat or T2DM-induced Nrf2 pathway impairment, DEX can reduce OS injury and inhibit the disorder of lipid anabolism and protect liver function. This study provides a theoretical basis for the protection of liver function by DEX in clinical T2DM patients.
