AI Article Synopsis

  • The study aimed to assess how dexmedetomidine (DEX) protects against liver damage caused by total body radiation in mice and to investigate the underlying mechanisms.
  • The experiment involved 40 mice divided into four groups: a control group, a group receiving DEX, a radiation-only group, and a group receiving both radiation and DEX, with various measurements taken to evaluate liver health.
  • Results showed that DEX treatment reduced markers of liver injury and oxidative stress compared to the radiation-only group, indicating its protective role and possible involvement of specific proteins (Nrf2 and HO-1) in the process.

Article Abstract

Background: The purpose of this study was to investigate the protective effects of dexmedetomidine (DEX) on total body radiation-induced acute liver injury in mice and to explore the possible mechanisms.

Methods: A total of 40 mice were randomly divided into the Control group (Group C), Dexmedetomidine group (Group Dex), Radiation group (Group R), and Group R+Dex. Mice in Group Dex and Group R+Dex were intraperitoneally injected with 10 µg/mL Dex at 50 mg/kg. Both Group C and Group R received normal saline instead of Dex. Mice were treated via continuous administration for 10 days and injection once a day (pre-administration for 3 days and 7 days after radiation). One hour after administration on the third day, the mice in Group R and R+Dex received total body radiation with a total dose of 6 Gy at a rate of 2 Gy/min. Group C received sham radiation. Levels of aspartate aminotransferase (AST), serum alanine aminotransferase (ALT), and liver levels of tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA) were measured. HE staining was employed to evaluate the pathological changes in liver tissues, and the expressions of Nrf2 and HO-1 proteins in the liver were measured by western blot.

Results: Compared with group C, serum levels of AST and ALT, liver TNF-α, IL-1β, MDA, and ROS levels increased, and SOD decreased in Group R. Group R mice had higher liver injury scores, and the protein expressions of Nrf2 and HO-1 proteins were lower (p < 0.05). Compared with Group R, the levels of AST, ALT, TNF-α, IL-1β, MDA, and ROS decreased, SOD increased, liver injury scores were lower, and the expressions of Nrf2 and HO-1 proteins were higher in the Group R+Dex group (all p < 0.05).

Conclusions: Dex exhibits a protective effect on reducing acute radiation-induced liver injury and oxidative stress, and the mechanism may be associated with the activation of Nrf2/HO-1 pathways.

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Source
http://dx.doi.org/10.7754/Clin.Lab.2022.220310DOI Listing

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