Differential JNK, p38 and ERK response to renal injury in a rat model of acute pancreatitis in pregnancy.
Arch Gynecol Obstet
; 297(4): 933-942, 2018 04.
Article
em En
| MEDLINE
| ID: mdl-29349553
ABSTRACT
OBJECTIVE:
The objective of this study was to determine the mechanism of acute renal injury (ARI) in acute necrotizing pancreatitis in late pregnancy (ANPIP).METHODS:
Pregnant Sprague-Dawley rats in the third trimester were used for this study, and an ANPIP model was induced by injecting 5% sodium taurocholate into the biliary pancreatic duct. The rats were randomly divided into three groups the normal, sham-operated (SO) and acute necrotizing pancreatitis (ANP) groups. Rats were killed at 3, 6, 12 h after the operation, and blood, pancreatic and renal tissue samples were harvested. Differences were detected in the physiology, pathology and cellular and molecular responses among the different groups.RESULT:
Serum amylase, lipase, urea and Cr levels were increased in rats with ANPIP. Additionally, expression of phosphorylation p38 and JNK as well as TNF-α and NF-κB were increased in the renal tissues of rats with ANPIP. The expression of phosphorylation ERK was decreased in the renal tissues of rats with ANPIP.CONCLUSIONS:
Mitogen-activated protein kinases may play an important role in renal injury in rat models of ANPIP.Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Ácido Taurocólico
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NF-kappa B
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Fator de Necrose Tumoral alfa
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Pancreatite Necrosante Aguda
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Proteínas Quinases JNK Ativadas por Mitógeno
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Proteínas Quinases p38 Ativadas por Mitógeno
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Injúria Renal Aguda
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
China