SUN Ke,CHEN Yong,LIU Zuo-jin,CHEN Zhen-zhen,LI Jin-zheng,HUANG Qing-yong,GONG Jian-ping,LIU Chuan.Protective mechanisms of IRAK-4 inhibited by taurine preconditioning in liver graft ischemia/reperfusion injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(11):1017-1020.
SUN Ke,CHEN Yong,LIU Zuo-jin,CHEN Zhen-zhen,LI Jin-zheng,HUANG Qing-yong,GONG Jian-ping,LIU Chuan.Protective mechanisms of IRAK-4 inhibited by taurine preconditioning in liver graft ischemia/reperfusion injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(11):1017-1020.DOI:
Objective To observe the changes in interleukin-1 receptor associated kinase-4 (IRAK-4) in ischemia/reperfusion (I/R) liver preconditioned with taurine and to explore the protective mechanisms of taurine preconditioning against hepatic I/R injury after liver transplantation. Methods Male Sprague-Dawley rats
weighing 180-220 g
were randomized into two groups in a blind fashion: control
normal saline group (NS group)
and taurine preconditioning group (TA group). After organ harvest
standardized liver transplantation was performed. At 0
60 min and 180 min after reperfusion
and the liver tissue IRAK-4 gene and protein level were determined by real-time quantitative fluorogenic PCR (FQ-PCR) and Western blotting. The activity of NF-κB in liver tissue was determined by electrophoretic mobility shift assay (EMSA). The serum tumor necrosis factor-α (TNF-α) level was detected by ELISA. Serum transaminases
liver histology
graft and animal survivals were also investigated. Results Taurine preconditioning greatly enhanced the one-week survival rate (P0.01)
improved graft function
and ameliorated the histopathologic signs of injury. The liver tissue IRAK-4 mRNA expression level
NF-κB binding activity
and TNF-α production in TA group were significantly lower than those in NS group (P0.01). Conclusion The findings from our study suggest that taurine can protect hepatic I/R injury after liver transplantation and the protective effects may be via down-regulation of IRAK4 and its downstream NF-κB and TNF-α expression.