| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5729264 | Transplantation Proceedings | 2017 | 7 Pages |
â¢This is the first experimental study to investigate the effects of tBHQ administered intravenously before a period of segmental hepatic I/R injury in rats.â¢tBHQ may modulate the I/R-induced Keap1/Nrf2/ARE signaling pathway activation and may prevent the development of injury after hepatic I/R by anti-oxidant and anti-apoptotic effects of tBHQ.â¢tBHQ alleviated I/R injury in rats, and it is reasonable to establish therapeutic function of tBHQ to oppose I/R-induced injury.
BackgroundHepatic ischemia/reperfusion (I/R) injury is a serious complication that occurs in surgical operations such as hepatectomy and liver transplantation. NF-E2-related factor 2 (Nrf2) is a transcription factor that has been proven against inflammatory and oxidative injury. Tert-butylhydroquinone (tBHQ), a widely used Nrf2 activator, is a common food preservative. In this study, we attempt to investigate the potential protective role of tBHQ in hepatic I/R injury.MethodsTwenty adult male rats were randomly divided into four groups: (1) sham+vehicle group; (2) I/R+vehicle group; (3) sham+tBHQ group; and (4) I/R+tBHQ group. The vehicle or tBHQ was divided into three injections at intervals of 12 hours in a model of hepatic I/R injury. Fluorescence quantitative polymerase chain reaction and Western blot analysis were used to examine Nrf2 mRNA and protein expression. The concentrations of malondialdehyde and superoxide dismutase activity were accessed, respectively.ResultsCompared with the sham+vehicle group, Nrf2 expression, malondialdehyde, content and serum alanine aminotransferase were significantly increased in the I/R+vehicle group, whereas superoxide dismutase activity was significantly decreased. However, in the I/R+tBHQ group, tBHQ ameliorated tissue damage; promoted glutathione-S-transferase, quinine oxidoreductase 1, and glutamate cysteine ligase inductions; and regained redox homeostasis in comparison with the I/R+vehicle group. Furthermore, the present study indicated that preconditioning with tBHQ suppressed the I/R-induced increase in the apoptotic protein levels of caspase-3, as well as the I/R-induced decrease in the levels of anti-apoptotic protein bcl-2.Conclusionst-BHQ exerted potent anti-inflammatory effects in I/R-induced liver injury, and tBHQ would be a new effectively therapeutic measure for preventing hepatic I/R injury during liver surgery.
