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1.
Chinese Journal of Contemporary Pediatrics ; (12): 285-287, 2011.
Article Dans Chinois | WPRIM | ID: wpr-308810

Résumé

<p><b>OBJECTIVE</b>To study the effects of TNF-α on ICAM-1 and LFA-1 expression in peripheral blood mononuclear cells (PBMC) of children with febrile seizures (FS).</p><p><b>METHODS</b>Sixteen children with FS and 16 age- and gender-matched healthy children were enrolled. The samples of PBMC from FS children were randomized into two groups with or without TNF-α treatment (TNF-α concentration 1.0 ng/mL). PBMC were purified and cultured with a conventional method in vitro. The expression of ICAM-1 and LFA-1 in PBMC was determined by flow cytometry (FCM).</p><p><b>RESULTS</b>ICAM-1[(20±9)% vs (14±7)%)]and LFA-1[(43±16)% vs (30±16)%]expression in PBMC in the untreated FS group was significantly higher than that in the normal control group (P<0.05). Compared with the untreated FS group, the treatment with TNF-α remarkably increased the ICAM-1 expression[(27±11)%](P<0.05). PBMC LFA-1 expression[(52±21)%]in the TNF-α-treated group was higher than that in the untreated FS group, although there were no statistical differences between the two groups.</p><p><b>CONCLUSIONS</b>TNF-α treatment may increase LFA-1 and ICAM-1 expression in PBMC of children with FS.</p>


Sujets)
Enfant , Enfant d'âge préscolaire , Femelle , Humains , Nourrisson , Mâle , Molécule-1 d'adhérence intercellulaire , Sang , Agranulocytes , Chimie , Antigène-1 associé à la fonction du lymphocyte , Sang , Crises convulsives fébriles , Allergie et immunologie , Facteur de nécrose tumorale alpha , Pharmacologie
2.
Chinese Journal of Hepatology ; (12): 368-373, 2009.
Article Dans Chinois | WPRIM | ID: wpr-310084

Résumé

<p><b>OBJECTIVE</b>To explore the therapeutic effect and mechanism of emodin on cholestatic hepatitis.</p><p><b>METHODS</b>Rats were divided into 5 groups: 1 group was untreated, the other 4 groups were treated with alpha-naphthylisothiocyanate (ANIT), ANIT and emodin, ANIT and ursodeoxycholic acid, or ANIT and dexamethasone, respectively. At 24 h, 48 h and 72 h after the treatment, NF-kappa B, early growth response factor-1 (Egr-1), cytokine-induced neutrophil chemoattractant 1 (CINC-1), macrophage inflammatory protein 2 (MIP-2), intercellular adhesion molecule 1 (ICAM-1),tumor necrosis factor alpha (TNF alpha) and interleukin-6 (IL-6) were assayed by immunohistochemistry, real-time PCR , western-blot and ELISA. The level of malondialdehyde (MDA), superoxide Dismutase(SOD) and myeloperoxidase (MPO) were assayed by thiobarbituric acid method, xanthine oxidase method and colorimetric method, respectively.</p><p><b>RESULTS</b>(1) Compared to the controls, emodin had a notable effect on total bilirubin (TB), direct bilirubin (DB), alanine aminotransferase (ALT) at all time points (all P less than 0.05). Compared to ursodeoxycholic acid, emodin had a notable effect on TB and DB at 24 h after the treatments, however, after 48 h, emodin had a notable effect only on TB (all P less than 0.05). Compared to Dexamethasone, emodin had a notable effect on TB at 48 h time point, and it had a notable effect on ALT at all time points (all P less than 0.05). (2) The nuclei NF-kappa B p65 staining was significantly increased at 24 h and 48 h after ANIT treatment (all P less than 0.05), and emodin treatment could block the increase (all P less than 0.05). (3) Egr-1 mRNA level was not affected by emodin treatment (P more than 0.05); levels of CINC-1, MIP-2 mRNA and ICAM-1 protein were significantly decreased after emodin treatment (all P less than 0.05). (4) The levels of TNF alpha and IL-6 were decreased after emodin treatment(all P less than 0.05). (5) The levels of MDA at all time points and MPO at 24 h, 48 h time points were notably down-regulated by emodin treatment, while the level of SOD was markedly elevated at all time points after emodin treatment (all P less than 0.05).</p><p><b>CONCLUSIONS</b>Emodin treatment can reduce the levels of TB, DB and ALT in ANIT induced-cholestatic hepatitis. The effect may be due to inhibition of NF-kappa B signal pathway.</p>


Sujets)
Animaux , Mâle , Rats , 1-Naphtyl-isothiocyanate , Anti-inflammatoires , Pharmacologie , Utilisations thérapeutiques , Lésions hépatiques dues aux substances , Traitement médicamenteux , Métabolisme , Cholestase intrahépatique , Traitement médicamenteux , Métabolisme , Facteur de transcription EGR-1 , Génétique , Métabolisme , Émodine , Pharmacologie , Utilisations thérapeutiques , Immunohistochimie , Molécule-1 d'adhérence intercellulaire , Métabolisme , Interleukine-6 , Métabolisme , Foie , Métabolisme , Anatomopathologie , Tests de la fonction hépatique , Facteur de transcription NF-kappa B , Métabolisme , ARN messager , Génétique , Métabolisme , Rat Sprague-Dawley , Transduction du signal , Facteur de nécrose tumorale alpha , Métabolisme
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