| Background and objectives:Critically ill newborn is the emergent patient in neonatal department and one of the most important factors leads to death of neonate and disability of children.With the development of medical techniques,mortality of newborn decreased over the past few years , but it remained 22.8‰in China in 2000. The underlying mechanisms for this phenomenon remain largely unknown.Researches have shown that disorder of immunological dysfunction involved in the severe illness,especial in the process of MOF. Studies also found melatonin which was produced mainly by human pineal gland was an immunological regulator. So we want to explore the effects of MT to the PBMC of critically ill newborn on the Th1/Th2 balance, NF-κB and so on. It is helpful to make clear the immunological mechanism of critically ill neonate and to seek an effective drug.Methods:Blood from 50 critically ill newborn and 25 healthy neonates were assessed. PBMC of critically ill newborn were divided into two groups,one group stimulated with PHA(critically ill group) and the other group stimulated with PHA + MT (MT group).For levels 0f NF-κB by EMSA cultured in vitro for 1 hours; levels 0f IFN-γ,IL-4 and TNF-αin the supernatants of PBMC by ELISA after cultured in vitro for 48 hours. PBMC of 25 healthy neonates were stimulated only PHA (control group).Results:1 Compared with control group,NF-κB of the critically ill group were activated(P<0.01) and the cytokine were disordered,IL-4 and TNF-αincreased,but IFN-γdecreased,also the ratio of IFN-γ/IL-4 is lower(p<0.01).2 Compared with critically ill group, the levels of NF-κB and TNF-αof MT group were statically lower (p<0.01), while IFN-γand IL-4 weren't changed (p>0.05).Conlusions:1 There is imblance of Th1/Th2 in newborn with critically illness.Th2 function prevails over the Th1 function and the levels of TNF-αincrease. NF-κB which promotes these cytokines is involved in the process of infants with criically illness.2 MT can improve the immunological function of critically ill newborn through partly attenuating activation of NF-κB signal transduction pathway and decrease the levels of TNF-αbut can't influence Th1/Th2 . |