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1.
Chinese Journal of Contemporary Pediatrics ; (12): 285-287, 2011.
Artigo em Chinês | WPRIM | ID: wpr-308810

RESUMO

<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>


Assuntos
Criança , Pré-Escolar , Feminino , Humanos , Lactente , Masculino , Molécula 1 de Adesão Intercelular , Sangue , Leucócitos Mononucleares , Química , Antígeno-1 Associado à Função Linfocitária , Sangue , Convulsões Febris , Alergia e Imunologia , Fator de Necrose Tumoral alfa , Farmacologia
2.
Chinese Journal of Hepatology ; (12): 368-373, 2009.
Artigo em Chinês | WPRIM | ID: wpr-310084

RESUMO

<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>


Assuntos
Animais , Masculino , Ratos , 1-Naftilisotiocianato , Anti-Inflamatórios , Farmacologia , Usos Terapêuticos , Doença Hepática Induzida por Substâncias e Drogas , Tratamento Farmacológico , Metabolismo , Colestase Intra-Hepática , Tratamento Farmacológico , Metabolismo , Proteína 1 de Resposta de Crescimento Precoce , Genética , Metabolismo , Emodina , Farmacologia , Usos Terapêuticos , Imuno-Histoquímica , Molécula 1 de Adesão Intercelular , Metabolismo , Interleucina-6 , Metabolismo , Fígado , Metabolismo , Patologia , Testes de Função Hepática , NF-kappa B , Metabolismo , RNA Mensageiro , Genética , Metabolismo , Ratos Sprague-Dawley , Transdução de Sinais , Fator de Necrose Tumoral alfa , Metabolismo
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