BACKGROUND: Brain-dead donors are the main sources for organ transplantation, but many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in BA-Ma mini pigs and the protective effects of breviscapine on hepatic function and on PKC-α mRNA and its protein expression.
METHODS: Fifteen BA-Ma mini pigs were equally divided into 3 groups at random: brain-dead (group B), breviscapine pretreated (group P), and control (group C). The brain-dead model was established by increasing intracranial pressure in a modified, slow and intermittent way. At 3, 6, 12, 18 and 24 hours after the initial brain-death, the levels of serum AST, ALT, TNF-α, IL-1β, and IL-6 were determined. The changes in hepatic tissues were assessed, and the expression of PKC-α and PKC-α mRNA was detected by immunohistochemistry and RT-PCR, respectively.
RESULTS: The levels of AST and ALT in groups B and P began to increase 12 hours after brain-death, while the values in group P were lower than those in group B (P<0.05). The levels of IL-1β, IL-6, and TNF-α in groups B and P at 3, 6, 12 and 18 hours were lower than those in group B (P<0.05). At 6, 12 and 24 hours, the expressions of PKC-α mRNA and PKC-α protein in group P were lower than those in group B (P<0.05). The degree of injury to hepatic cells in group P was milder than that in group B.
CONCLUSIONS: Breviscapine inhibits the degree of PKC-α mRNA transcription and its protein translation, decreases the release of inflammatory factors, and thus alleviates hepatic injury during brain-death.