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1.
Allergol. immunopatol ; 40(4): 238-243, jul.-ago. 2012. tab, graf, ilus
Artigo em Inglês | IBECS | ID: ibc-101277

RESUMO

Background and aims: Activation of the pro-inflammatory and anti-inflammatory cytokine cascade, including tumour necrosis factor (TNF)-alpha and interleukin (IL)-4, is considered to play an important role in severe liver injury. Kupffer cells, resident macrophages of the liver, activated with lipopolysaccharide (LPS) release pro-inflammatory cytokine. d-Galactosamine (d-GalN), a hepatocyte-specific inhibitor of RNA synthesis, is known to sensitise animals to the lethal effects of LPS. In the present study we seek to reverse some altered parameters, immunological and histopathological, to normal values of rats pre-treated with garlic. Methods: Acute hepatic failure was induced in male albino rats by the intraperitoneal injection of 500 mg d-GalN and 50 microg LPS/kg body weight. Expression levels of TNF-alpha and IL-4 were detected by ELISA. Leukocytes proliferation was carried out by differential count. For histopathology, liver sections were stained with haematoxylin and eosin. Data were analysed by SPSS program version 13.0. Results: The data showed significant increase in the numbers of granulocytes, but with significant decreases in lymphocyte and monocytes proliferation and the TNF-alpha and IL-4 levels ind-GalN/LPS-induced group. Garlic pre-treatment of liver-injured rats induced significant amelioration in the numbers of monocytes and lymphocytes, with significant increase in granulocytes numbers, TNF-alpha level and IL-4 level. Conclusions: Results of this study revealed that garlic could afford a significant protection in the alleviation of d-GalN/LPS-induced hepatocellular injury(AU)


Assuntos
Animais , Ratos , Insuficiência Hepática/tratamento farmacológico , Alho , Extratos Vegetais/farmacocinética , Ratos , Modelos Animais de Doenças , Galactosamina/efeitos adversos , Lipopolissacarídeos/efeitos adversos , Granulócitos , Leucócitos
2.
Allergol Immunopathol (Madr) ; 40(4): 238-43, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22280552

RESUMO

BACKGROUND AND AIMS: Activation of the pro-inflammatory and anti-inflammatory cytokine cascade, including tumour necrosis factor (TNF)-alpha and interleukin (IL)-4, is considered to play an important role in severe liver injury. Kupffer cells, resident macrophages of the liver, activated with lipopolysaccharide (LPS) release pro-inflammatory cytokine. D-Galactosamine (D-GalN), a hepatocyte-specific inhibitor of RNA synthesis, is known to sensitise animals to the lethal effects of LPS. In the present study we seek to reverse some altered parameters, immunological and histopathological, to normal values of rats pre-treated with garlic. METHODS: Acute hepatic failure was induced in male albino rats by the intraperitoneal injection of 500 mg D-GalN and 50 µg LPS/kg body weight. Expression levels of TNF-α and IL-4 were detected by ELISA. Leukocytes proliferation was carried out by differential count. For histopathology, liver sections were stained with haematoxylin and eosin. Data were analysed by SPSS program version 13.0. RESULTS: The data showed significant increase in the numbers of granulocytes, but with significant decreases in lymphocyte and monocytes proliferation and the TNF-alpha and IL-4 levels in D-GalN/LPS-induced group. Garlic pre-treatment of liver-injured rats induced significant amelioration in the numbers of monocytes and lymphocytes, with significant increase in granulocytes numbers, TNF-α level and IL-4 level. CONCLUSIONS: Results of this study revealed that garlic could afford a significant protection in the alleviation of D-GalN/LPS-induced hepatocellular injury.


Assuntos
Alho/química , Falência Hepática Aguda/terapia , Fitoterapia/métodos , Animais , Contagem de Células , Proliferação de Células , Células Cultivadas , Galactosamina , Interleucina-4/metabolismo , Leucócitos , Lipopolissacarídeos , Fígado/imunologia , Fígado/patologia , Falência Hepática Aguda/induzido quimicamente , Falência Hepática Aguda/patologia , Masculino , Ratos , Ratos Endogâmicos , Fator de Necrose Tumoral alfa/metabolismo
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