2002•Shanghai yixueRequires access

The role of nuclear factor-kappa B in the pathogenesis of severe acute pancreatitis-associated hepatic injury

Zhu Yin

Open publisher page 1 citations

Abstract

Objective To investigate the role of NF κB (nuclear factor kappa B) in the pathogenesis of severe acute pancreatitis associated hepatic injury. Methods Thirty eight feamle Wistar rats were divided into SAP group and PDTC pretreated group and normal group. Pancreatitis was induced by intraductal administration of 5% sodium taurocholate. Pyrrolidine dithiocarbamate (PDTC) pretreated SAP rats were given 100 mg/kg PDTC intraperioneally before pancreatitis was induced. Rats in SAP group and PDTC pretreated group were killed 3, 6, 12 hours after induction of the model. We detected the blood AST, and observed the liver tissue stained by H E, and the NF κB activity in liver tissue was detected by immunohistochemical methods. The mRNA expression of TNF α、IL 6、ICAM 1 in the liver was evaluated by reverse transcription polymerase chain reaction.Results The liver tissue stained by H E in SAP group had little change, there was no liver cells necrosis or apoptosis. Blood AST increased significantly in SAP group comparing with the normal group. The activity of NF κB and the levels of TNF α、IL 6 increased significantly in liver tissue of the SAP group, but there was no change in ICAM 1mRNA. PDTC was found to decrease the levels of AST, TNF α、IL 6 and NF κB activity in liver tissue. Conclusion Hepatic injury is present in SAP, which is caused by upregulation of TNF α, IL 6 mRNA expression induced by NF κB, it is possible that inhibition of NF κB activity may be a promising strategy in the treatment of SAP by downregulating the above cytokines.

About this research paper

What this paper is about

Objective To investigate the role of NF κB (nuclear factor kappa B) in the pathogenesis of severe acute pancreatitis associated hepatic injury. Methods Thirty eight feamle Wistar rats were divided into SAP group and PDTC pretreated group and normal group. Pancreatitis was induced by intraductal administration of 5% sodium taurocholate. Pyrrolidine dithiocarbamate (PDTC) pretreated SAP rats were given 100 mg/kg PDTC intraperioneally before pancreatitis was induced. Rats in SAP group and PDTC pretreated group were killed 3, 6, 12 hours after induction of the model. We detected the blood AST, and observed the liver tissue stained by H E, and the NF κB activity in liver tissue was detected by immunohistochemical methods. The mRNA expression of TNF α、IL 6、ICAM 1 in the liver was evaluated by reverse transcription polymerase chain reaction.Results The liver tissue stained by H E in SAP group had little change, there was no liver cells necrosis or apoptosis. Blood AST increased significantly in SAP group comparing with the normal group. The activity of NF κB and the levels of TNF α、IL 6 increased significantly in liver tissue of the SAP group, but there was no change in ICAM 1mRNA. PDTC was found to decrease the levels of AST, TNF α、IL 6 and NF κB activity in liver tissue. Conclusion Hepatic injury is present in SAP, which is caused by upregulation of TNF α, IL 6 mRNA expression induced by NF κB, it is possible that inhibition of NF κB activity may be a promising strategy in the treatment of SAP by downregulating the above cytokines.

Why it matters

OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective To investigate the role of NF κB (nuclear factor kappa B) in the pathogenesis of severe acute pancreatitis associated hepatic injury. Methods Thirty eight feamle Wistar rats were divided into SAP group and PDTC pretreated group and normal group. Pancreatitis was induced by intraductal administration of 5% sodium taurocholate. Pyrrolidine dithiocarbamate (PDTC) pretreated SAP rats were given 100 mg/kg PDTC intraperioneally before pancreatitis was induced. Rats in SAP group and PDTC pretreated group were killed 3, 6, 12 hours after induction of the model. We detected the blood AST, and observed the liver tissue stained by H E, and the NF κB activity in liver tissue was detected by immunohistochemical methods. The mRNA expression of TNF α、IL 6、ICAM 1 in the liver was evaluated by reverse transcription polymerase chain reaction.Results The liver tissue stained by H E in SAP group had little change, there was no liver cells necrosis or apoptosis. Blood AST increased significantly in SAP group comparing with the normal group. The activity of NF κB and the levels of TNF α、IL 6 increased significantly in liver tissue of the SAP group, but there was no change in ICAM 1mRNA. PDTC was found to decrease the levels of AST, TNF α、IL 6 and NF κB activity in liver tissue. Conclusion Hepatic injury is present in SAP, which is caused by upregulation of TNF α, IL 6 mRNA expression induced by NF κB, it is possible that inhibition of NF κB activity may be a promising strategy in the treatment of SAP by downregulating the above cytokines.

Key concepts: Pyrrolidine dithiocarbamate, Medicine, Pathogenesis, Acute pancreatitis, Pancreatitis, Tumor necrosis factor alpha, Liver injury, Internal medicine

Related papers

Back to paper searchBrowse research topicsOriginal source
The role of nuclear factor-kappa B in the pathogenesis of severe acute pancreatitis-associated hepatic injury — Research Paper | ScholarLens