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1.
Chinese Journal of Contemporary Pediatrics ; (12): 198-200, 2006.
Article Dans Chinois | WPRIM | ID: wpr-262745

Résumé

<p><b>OBJECTIVE</b>This study investigated the serum levels of interleukin-5 (IL-5), leukotriene B4 (LTB4) and C-reactive protein (CRP) in children with Henoch-Schonlein purpura (HSP) at different phases to explore the role of IL-5, LTB4 and CRP in the pathogenesis of HSP.</p><p><b>METHODS</b>Serum levels of IL-5, LTB4 and CRP in 27 normal children and 31 children with HSP at the acute phase and the early recovery phase were detected using ELISA.</p><p><b>RESULTS</b>The serum levels of IL-5, LTB4 and CRP in children with HSP were 53.8 +/- 4.2 pg/mL, 95.3 +/- 12.0 pg/mL and 36.10 +/- 11.78 mg/L, respectively at the acute phase. The values were significantly decreased at the early recovery phase (37.8 +/- 3.9 pg/mL, 45.7 +/- 10.1 pg/mL, 18.35 +/- 6.43 mg/L; P < 0.01), but remained higher than those in normal controls (12.7 +/- 3.2 pg/mL, 17.6 +/- 5.7 pg/mL, 4.75 +/- 2.85 mg/L; P < 0.01). The serum levels of IL-5 and LTB4 positively correlated to the CRP level.</p><p><b>CONCLUSIONS</b>The serum levels of IL-5 and LTB4 in children with HSP increased during the acute phase and decreased at the early recovery phase, suggesting that IL-5 and LTB4 may be involved in the pathogenesis of HSP.</p>


Sujets)
Adolescent , Enfant , Enfant d'âge préscolaire , Femelle , Humains , Mâle , Protéine C-réactive , Interleukine-5 , Sang , Leucotriène B4 , Sang , , Sang
2.
Chinese Journal of Contemporary Pediatrics ; (12): 225-230, 2006.
Article Dans Chinois | WPRIM | ID: wpr-262738

Résumé

<p><b>OBJECTIVE</b>To investigate the protective effects of 15-methyl-lipoxin A4 (LXA4) on mesangioproliferative nephritis in rats and the possible mechanisms.</p><p><b>METHODS</b>Mesangioproliferative nephritis was induced by a single intravenous injection of the mouse monoclonal anti-Thy1.1 antibodies (ER4) in 20 rats. Ten nephritic rats were injected with 15-methyl-LXA4 at 10 minutes before ER4 antibody injection and then 8-hourly until the rats were sacrificed on day 4 after nephritis induction. The nephritis was evidenced by presence of proteinuria, histologic examination with light microscopy, infiltrating leukocyte assessed by immunofluorescence microscopy, and mesangial cell proliferation assessed by proliferation scoring and by immunohistochemical staining of proliferating cell nuclear antigen (PCNA). Expressions of interleukin (IL)-1beta and IL-6 protein or mRNA in glomeruli were determined by radioimmunoassay or RT-PCR, respectively. Phosphorylated phosphoinositide 3-kinase (PI3-K), Akt1 and p27(kip1) in glomeruli were analyzed by Western Blot. Activities of nuclear factor-kappaB (NF-kappaB) and signal transducer and activator of transcription 3 (STAT3) in glomeruli were assessed by electrophoretic mobility shift assay (EMSA).</p><p><b>RESULTS</b>There were increases in glomerular infiltration of leukocyte, expressions of IL-1beta and IL-6 protein and mRNA, and activities of NF-kappaB in nephritic rats between days 1 and 4 after nephritis induction. The enhanced proteinuria, score of mesangial proliferation, glomerular PCNA positive cells, activities of phosphorylated PI3-K, Akt1 and STAT3, and reduced p27(kip1) expression were found on day 4 after nephritis induction. 15-Methyl-LXA4 treatment significantly reduced the proteinuria, glomerular infiltration of leukocyte, expressions of IL-1beta and IL-6 protein and mRNA, score of mesangial proliferation, glomerular PCNA positive cells, activities of phosphorylated PI3-K, Akt1, NF-kappaB and STAT3, and increased the p27(kip1) expression.</p><p><b>CONCLUSIONS</b>15-Methyl-LXA4 can markedly inhibit the proteinuria, glomerular inflammation, and mesangial cell proliferation induced by anti-Thy1.1 antibodies. The inhibition effects are related to PI3-K/Akt1/p27(kip1)/cyclin pathway, STAT3 and NF-kappaB pathway-dependent signal transduction.</p>


Sujets)
Animaux , Femelle , Rats , ADN , Métabolisme , Glomérulonéphrite membranoproliférative , Traitement médicamenteux , Interleukine-1 , Génétique , Interleukine-6 , Génétique , Lipoxines , Utilisations thérapeutiques , Facteur de transcription NF-kappa B , Métabolisme , Phosphatidylinositol 3-kinases , Physiologie , ARN messager , Rats de lignée LEW , Facteur de transcription STAT-3 , Métabolisme , Transduction du signal
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