EXPRESSION OF IκBα IN PERIPHERAL BLOOD MONO-NUCLEAR
CELLS OF CHILDREN WITH STEROID RESPONSIVE SIMPLE NEPHROTIC SYNDROME AND
ROLE OF TRANSCRIPTIONAL ACTIVATION IκBα IN MEDIATION IMMUNOSUPPRESSION
BY GLUCOCORTOIDS
Tao Y-H, Wang Z, Li C-S, Zhu X-S
Department of Pediatrics, the Second Hospital, West China Medical Center,
Sichuan University, Chengdu, China
Objective: To study modulation
mechanism of activation of nuclear factor kappaB (NF-κB) in triggering steroid response simple nephrotic
syndrome (SRSNS) via detecting the inhibitory KappaB alpha (IκBα) expression in peripheral blood cells (PBMCs)
in children with nephrotic syndrome and investigating its relationship with
NF-κB .To attempt to
comprehend the role of action IκBαin suppression by glucocortoids.
Methods: The
expression of IκBα was detected by real-time fluorescence reverse
transcriptase-PCR (RT-PCR) and western blot analysis. Expression of NF-κB
was measured by electrophretic mobility shift assay.
Results: The
expression of IκBα in PBMCs from children with SNSRS in active stage was
lower than not only that of nephritis nephrotic syndrome and secondary
nephrotic syndrome in active stage but that of normal controls and children
with SNSRS in remission stage (P<0.05). Statistically, there is no
significant difference between the expression of IκBα in PBMCs from
children with SNRS in remission stage and that from normal controls
(P>0.05). Following glucocortoid therapy, the expression of IκBα in
PBMCs from children with SNSRS elevated significant statistically
(P<0.05). Otherwise, a negative correlation lied in the expression of
IκBα and that of NF-κB (r= -0.87) .
Conclusions: Reduced
IκBα expression in PBMCs of children in active stage has involved in the
activation of NF-κB, which may be one of the most important ways of
triggering SRSNS by respiratory tract viruses. It is shown that
glucocortoids induces the transcription of the IκBα gene, which results in
increasing IκBα protein syntheses and reducing the activation of NF-κB.