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Mucosal expression of defensin-5, soluble phospholipase A2 and lysozyme in the intestine in a rat model of acute liver failure and its relationship to intestinal bacterial translocation / Expresión de defensina-5, fosfolipasa A2 soluble y lisozima en la mucosa intestinal en un modelo de rata con insuficiencia hepática aguda y su relación con la traslocación bacteriana intestinal
Chen, Silin; Li, Xiaopeng; Li, Ming; Mei, Qing; Huang, Juanjun; Wu, Zhenping; Zhang, Lunli.
Afiliação
  • Chen, Silin; First Affiliated Hospital of Nanchang University. Department of Infectious Diseases. Jiangxi. China
  • Li, Xiaopeng; First Affiliated Hospital of Nanchang University. Department of Infectious Diseases. Jiangxi. China
  • Li, Ming; Key Laboratory of Liver Regeneration Medicine. Jiangxi. China
  • Mei, Qing; Jing Zhou Central Hospital. Department of Ultrasound. Hubei. china
  • Huang, Juanjun; Ganzhou People's Hospital. Department of Infectious Diseases. Jiangxi. China
  • Wu, Zhenping; First Affiliated Hospital. Zhejiang University School of Medicine. Zhejiang. China
  • Zhang, Lunli; First Affiliated Hospital of Nanchang University. Department of Infectious Diseases. Jiangxi. China
Gastroenterol. hepatol. (Ed. impr.) ; 43(6): 293-300, jun.-jul. 2020. ilus, tab, graf
Artigo em Inglês | IBECS | ID: ibc-193511
Biblioteca responsável: ES1.1
Localização: BNCS
ABSTRACT

INTRODUCTION:

To study the expression of defensin-5 (RD-5), soluble phospholipase A2 (sPLA2) and lysozyme in the intestine in a rat model of acute liver failure and its relationship with intestinal bacterial translocation (BT). PATIENTS AND

METHODS:

Sprague-Dawley (SD) rats were divided into two groups. The experimental group was divided into five subgroups according to the lapsing time after the model was established, which were designated accordingly as 8 h, 16 h, 24 h, 48 h, and 72 h groups. Acute liver failure (ALF) model was induced by intraperitoneal injection of 10% d-galactosamine. The homogenates of mesenteric lymph nodes (MLNs), liver and spleen from each group were cultured in agar to determine the bacterial outgrowth. The mRNA expression of RD-5, sPLA2, lysozyme and the protein expression of sPLA2, lysozyme were determined.

RESULTS:

No bacteria grew in the organ cultures from the control group while experimental groups had positive cultures. Expression of the RD-5 and sPLA2 mRNA in the experimental groups gradually increased at early time points and peaked 16 h after induction of ALF, then progressively decreased. The mRNA expression of lysozyme in the experimental group peaked at 8 h after ALF induction, then progressively decreased. Similar results were obtained with Western blot and immunohistochemical staining.

DISCUSSION:

The immune barrier function of the ileal mucosa in the rat model of acute liver failure was compromised as demonstrated by the decreased expression of RD-5, sPLA2 and lysozyme in Paneth cells along with increased intestinal bacterial translocation
Assuntos
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Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Muramidase / Falência Hepática Aguda / Translocação Bacteriana / Defensinas / Mucosa Intestinal Limite: Animais Idioma: Inglês Revista: Gastroenterol. hepatol. (Ed. impr.) Ano de publicação: 2020 Tipo de documento: Artigo Instituição/País de afiliação: First Affiliated Hospital of Nanchang University/China / First Affiliated Hospital/China / Ganzhou People's Hospital/China / Jing Zhou Central Hospital/china / Key Laboratory of Liver Regeneration Medicine/China
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Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Muramidase / Falência Hepática Aguda / Translocação Bacteriana / Defensinas / Mucosa Intestinal Limite: Animais Idioma: Inglês Revista: Gastroenterol. hepatol. (Ed. impr.) Ano de publicação: 2020 Tipo de documento: Artigo Instituição/País de afiliação: First Affiliated Hospital of Nanchang University/China / First Affiliated Hospital/China / Ganzhou People's Hospital/China / Jing Zhou Central Hospital/china / Key Laboratory of Liver Regeneration Medicine/China
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