Effect of emodin in suppressing acute rejection following liver allograft transplantation in rats / 中国结合医学杂志
Chin. j. integr. med
; Chin. j. integr. med;(12): 151-156, 2010.
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| ID: wpr-344933
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ABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of action of emodin for suppressing acute allograft rejection in a rat model of liver transplantation.</p><p><b>METHODS</b>Brown Norway (BW) recipient rats of orthotopic liver transplantation (OLT) were divided into three groups, Group A receiving isografting (with BW rats as donor), Group B receiving allografting (with Lewis rats as donor), Group C receiving allografting and emodin treatment (50 mg/kg daily). They were sacrificed on day 7 of post-transplantation, and their hepatic histology, plasma cytokine levels, and T-cell subset expression were detected.</p><p><b>RESULTS</b>Compared with those in Group A, rats: in Group B exhibited severe allograft rejection with a rejection activity index (RAI) of 7.67+/-0.98, extensive hepatocellular apoptosis with an apoptosis index (AI) of 35.83+/-2.32, and elevated plasma levels of interleukin-2 (IL-2), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-alpha), CD4(+) and CD4 CD4(+)/CD8(+) ratio. However, recipients in Group C showed a decrease in histological grade of rejection and hepatocellular apoptosis, as well as a decrease in plasma levels of IL-2, TNF-alpha, CD4(+) and CD4(+)/CD8(+) ratio, but elevated levels of IL-10 as compared with the allograft group.</p><p><b>CONCLUSION</b>Post-OLT acute rejection could be attenuated by emodin, its mechanism of action may be associated with protecting hepatocytes from apoptosis, polarizing the Th 1 paradigm to Th2, and inhibiting the proliferation of CD4(+) T cell in plasma.</p>
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Índice:
WPRIM
Assunto principal:
Patologia
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Farmacologia
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Ratos Endogâmicos Lew
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Ratos Endogâmicos BN
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Reabilitação
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Transplante Homólogo
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Sangue
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Doença Aguda
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Citocinas
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Subpopulações de Linfócitos T
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Chin. j. integr. med
Ano de publicação:
2010
Tipo de documento:
Article