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Role of p38 mitogen-activated protein kinase pathway on renal failure in the infant rat after burn injury.
Shock. 2004 Jun; 21(6):535-42.S

Abstract

The p38 mitogen-activated protein kinase (MAPK) pathway is a proinflammatory signal transduction pathway for the production of cytokines and cellular response to stress, such as bacterial LPS or ischemia. We examined the effects of FR167653, a specific inhibitor of p38 MAPK, to explore the relationship between intestinal barrier damage and remote renal dysfunction. Immunohistochemical data showed the accumulation of neutrophils in the intestine after burn, and a horseradish peroxidase (HRP) tracer experiment showed burn-induced intestinal barrier damage. Our quantitative bacterial culture data demonstrated that viable bacteria reached the remote organs after burn and prevented the invading viable bacteria from using FR167653. Western blotting identified increased phosphorylation of p38 MAPK in the kidney after burn, and it may also have shown the possibility that endotoxin associated with the bacterial translocation enhances the activation of the p38 MAPK pathway. We blocked the intestinal barrier damage using FR167653, which resulted in reduced neutrophils in the intestine. FR167653 also prevented the increased phosphorylation of p38 MAPK in the kidney, which resulted in reduced neutrophils in the glomerulus and the reduction of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta mRNA in the kidneys, and, finally, prevented burn-induced renal failure. This study provides evidence for the hypothesis that the p38 MAPK pathway controls inflammatory mediators and not only improves intestinal function but also reduces remote renal failure after burn. We identified the pathophysiologic role of the p38 MAPK pathway in the development of renal failure after burn.

Authors+Show Affiliations

Department of Forensic Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. kita@med.uoeh-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15167682

Citation

Kita, Toshiro, et al. "Role of P38 Mitogen-activated Protein Kinase Pathway On Renal Failure in the Infant Rat After Burn Injury." Shock (Augusta, Ga.), vol. 21, no. 6, 2004, pp. 535-42.
Kita T, Yamaguchi H, Sato H, et al. Role of p38 mitogen-activated protein kinase pathway on renal failure in the infant rat after burn injury. Shock. 2004;21(6):535-42.
Kita, T., Yamaguchi, H., Sato, H., Kasai, K., Tanaka, T., & Tanaka, N. (2004). Role of p38 mitogen-activated protein kinase pathway on renal failure in the infant rat after burn injury. Shock (Augusta, Ga.), 21(6), 535-42.
Kita T, et al. Role of P38 Mitogen-activated Protein Kinase Pathway On Renal Failure in the Infant Rat After Burn Injury. Shock. 2004;21(6):535-42. PubMed PMID: 15167682.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of p38 mitogen-activated protein kinase pathway on renal failure in the infant rat after burn injury. AU - Kita,Toshiro, AU - Yamaguchi,Hiroki, AU - Sato,Hiroaki, AU - Kasai,Kentaro, AU - Tanaka,Toshiko, AU - Tanaka,Noriyuki, PY - 2004/5/29/pubmed PY - 2005/2/16/medline PY - 2004/5/29/entrez SP - 535 EP - 42 JF - Shock (Augusta, Ga.) JO - Shock VL - 21 IS - 6 N2 - The p38 mitogen-activated protein kinase (MAPK) pathway is a proinflammatory signal transduction pathway for the production of cytokines and cellular response to stress, such as bacterial LPS or ischemia. We examined the effects of FR167653, a specific inhibitor of p38 MAPK, to explore the relationship between intestinal barrier damage and remote renal dysfunction. Immunohistochemical data showed the accumulation of neutrophils in the intestine after burn, and a horseradish peroxidase (HRP) tracer experiment showed burn-induced intestinal barrier damage. Our quantitative bacterial culture data demonstrated that viable bacteria reached the remote organs after burn and prevented the invading viable bacteria from using FR167653. Western blotting identified increased phosphorylation of p38 MAPK in the kidney after burn, and it may also have shown the possibility that endotoxin associated with the bacterial translocation enhances the activation of the p38 MAPK pathway. We blocked the intestinal barrier damage using FR167653, which resulted in reduced neutrophils in the intestine. FR167653 also prevented the increased phosphorylation of p38 MAPK in the kidney, which resulted in reduced neutrophils in the glomerulus and the reduction of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta mRNA in the kidneys, and, finally, prevented burn-induced renal failure. This study provides evidence for the hypothesis that the p38 MAPK pathway controls inflammatory mediators and not only improves intestinal function but also reduces remote renal failure after burn. We identified the pathophysiologic role of the p38 MAPK pathway in the development of renal failure after burn. SN - 1073-2322 UR - https://www.unboundmedicine.com/medline/citation/15167682/Role_of_p38_mitogen_activated_protein_kinase_pathway_on_renal_failure_in_the_infant_rat_after_burn_injury_ L2 - https://doi.org/10.1097/00024382-200406000-00007 DB - PRIME DP - Unbound Medicine ER -