Abstract
Objective To investigate the protective role of SP600125, a selective c-Jun N-terminal kinase inhibitor,in the apoptosis of cardiomyocytes in brain death rats. Methods Twenty Sprague-Dawley(SD) rats were randomly divided into:Sham group(n= 5), only given intracranial insertion of Fogarty tube after anesthesia; brain- death group(n= 5), given brain death for 6 h; SP600125 group (n= 5), given peritoneal injection of SP600125(10 mg/kg)1 h before brain death for 6 h; and DMSO group(n= 5), given peritoneal injection of placebo solution DMSO(10 mg/kg)1 h before brain death for 6 h.At 6 h, the apical myocardial samples were obtained for detection of Cysteinyl aspartate-specific protease(Caspase)- 3 and cytochrome- C(Cyt- C) mRNA and protein expression by real- time quantitative polymerase chain reaction(real- time PCR)and Western blotting respectively.Apoptosis of cardiac muscle cells was determined by terminal deoxynucleotidyl transferase d UTP nick end labelling(TUNEL) assay. Results (1)Real-time PCR showed that the mRNA expression of Caspase- 3 and Cyt- C mRNA in brain death group was(2.37±0.12, 2.03±0.08) times higher than that in sham group(P 0.05). The mRNA expression of Caspase-3 and Cyt- Cin SP600125 group(1.21±0.05 and 1.23±0.24)was significantly lower than that in brain death group(2.38±0.11 and 2.06±0.09)(P 0.05), and that in SP600125 group(39.45±5.73 and 20.34±5.69) was decreased significantly as compared with that in brain death group(P 0.05],and that in SP600125 group[(7.63±3.09)%]was significantly reduced as compared with that in brain death group(P< 0.05). Conclusion SP600125 played protective roles in the apoptosis of cardiomyocytes in brain death rats through specifically inhibiting the activity of JNK signaling pathway. Key words: Donor heart; Brain death; Apoptosis; c-Jun N-terminal kinase inhibitor
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call