Objective To investigate the changes of melatonin and cellular immunological function in children with febrile seizures and its clinical significance. Methods 50 children, including 23 cases with complex febrile seizure (CFS) and 27 cases with simple febrile seizure (SFS) , and 25 cases with upper respiratory infections children selected as control group were enrolled in this study. Serum melato- nin was measured by enzyme-linked immunosorbent assay (ELISA) and cellular immunological function was measured by flow eytomcter. Results The levels of serum melatonin in the 3 groups of CFS, SFS, control were(14. 91±2. 61) ng/L, (20. 72±2. 54) ng/L, (23.93± 2. Ol) ng/L, respectively. The melatonin levels in CFS children were significantly decreased than that in control group and SFS children (P <0. O1). CD3 + ,CD4 +, the ratio of CD4 + /CD8 + and CD8 + in CFS group were significantly decreased than that in control group and SFS group (P <0.01). The ratio of CD4 +/CD8 + in SFS group was significantly decreased than that in control group (P <0.05), but CD3 + ,CD4 + and CD8 + had no statistics significance among these groups(P >0. 05). The serum rnelatonin level were positive related withdecreaseddegreeofCD3+,CD4+ andtberatioofCD4+ /CDS+ (r≥0. 472, P <0.05). Conclusion The disorder cfcellular immunological function was possible related with the loss of serum melatonin, and the loss of serum melatonin maybe one of the reasons for febrile seizures relapse and brain injured.

ObjectiveTostudythemolecularmechanismoflanthanumonblocking lipopolysaccharide(LPS)-mediated activation of nuclear factor-kappaB (NF-κB)signaling in macrophages.MethodsThe RAW264.7 macrophages were cultured routinely and divided into 4 groups randomly:LaCl3 +LPS group,LPS group,LaCl3 group and control group.The nuclear translocation of p65 protein was detected by immunocytochemistry.Total,cytoplasmic and nuclear proteins were extracted respectively,and then the binding activity of p65 with the target gene was measured by ELISA.Western blot assays were also performed to detect the expression levels of the proteins,including nuclear p65,IκBα and IKK kinase,the phosphorylation status of IκBα and IKK kinase.ResultsLanthanum can block LPS-induced activation of p65 protein through various ways,such as inhibiting its nuclear translocation,reducing its expression in the nuclei and decreasing its binding activity with the target genes.Lanthanum inhibited the degradation of LPS-induced IκBα,but the phosphorylation of LPS-induced IKKβ can not be blocked by lanthanum,nor did the phosphorylation ability of p-IKKβ on IκBα.Conclusion Lanthanum inhibited the degradation of IκBα,nuclei translocation of p65 protein and its binding activity with the target genes,thereby inhibited LPS-induced NFκB activation,which might be one of the inhibition mechanisms of lanthanum on nuclear activation.