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Effect of free radical scavenger on c-jun activation in rats with crush syndrome
Wei Zhai1, Yun-Fei Xu, Bo Peng
1Department of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Objectives:
To evaluate the relationship between reactive oxygen species (ROS)-mediated kidney injuries and Jun N-terminal kinase (JNK) activity and the therapeutic effects of tempol in crush syndrome (CS) model rats.
Methods:
Male Wister rats were randomly divided into sham operation group (SOG), CS groups (CS6G, CS12G and CS24G) and tempol treatment group (TG, a ROS scavenger). CS model rats were established by crushing the hind limbs of rats with 15 kg pressure for 6 hours, and inferior caval vein blood and kidney samples were harvested at 6, 12, 24 hours after removing crush pressure. In TG, 100 mg/kg tempol was intraperitoneally injected into CS model rats after withdraw of crush pressure. In SOG, rats were fixed on the board without any crush pressure. The activation of c-jun was determined by western blotting. Serological parameters and the content of malondialdehyde (MDA) in kidney tissues were determined by standard methods.
Results:
Acute kidney injury reached the peak at 12 hours after the crush pressure. Compared with SOG, the content of phosphorylated c-jun was significantly higher in CSG and TG (p < 0.05), and the content of phosphorylated c-jun in the CSG was significantly higher than that in TG (p < 0.05). Interestingly, the changes of the MDA content in the kidney tissues of the 3 groups were similar to the changes of phosphorylated c-jun content.
Conclusion:
ROS-mediated phosphorylation of c-jun may play important roles in the acute kidney injury of CS rats. Tempol can inhibit the phosphorylation of c-jun and alleviate the acute kidney injury.
