These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Inhibition of NF-KB does not induce c-Jun N-terminal kinase-mediated apoptosis in reperfusion injury.
    Author: Rushing GD, Britt LD.
    Journal: J Am Coll Surg; 2007 May; 204(5):964-7; discussion 967-8. PubMed ID: 17481520.
    Abstract:
    BACKGROUND: The role of C-Jun N-terminal Kinase (c-Jun Kinase) in apoptosis is unclear. It is likely that c-Jun Kinase activation is cell type and stimulus dependent. c-Jun Kinase promotes tumor necrosis factor (TNF)-alpha mediated apoptosis in nuclear factor (NF)-KB deficient cells. Minimal NF-KB expression may be enough to abrogate c-Jun Kinase-mediated apoptosis during reperfusion injury. STUDY DESIGN: Forty Sprague-Dawley rats underwent hemorrhagic ischemia and reperfusion. Twenty experimental animals were treated with the NF-KB inhibitor herbimycin A, and 20 control animals underwent only hemorrhage and reperfusion. Serum TNF-alpha and c-Jun Kinase levels were measured. Adrenal, kidney, liver, ileum, colon, and skeletal muscle tissues were evaluated for apoptosis by hematoxylin and eosin staining. RESULTS: TNF-alpha levels were 400 pg/mL (control) and 385 pg/mL (experimental) during ischemia (p=0.46), increased in controls to 450 pg/mL, and decreased in the experimental arm to 175 pg/mL (p=0.028). c-Jun Kinase levels were 1,525 pg/mL (control) and 1,475 pg/mL (experimental) during ischemia (p=0.35) and increased to 5,250 pg/mL (control) and 5,000 pg/mL (experimental) after reperfusion (p=0.26). In control animals, necrosis was seen in kidney, adrenal, and liver specimens. Compared with controls, experimental animals had average tissue hemorrhage scores of less than 1 (p < 0.001), with no necrosis seen in any experimental arm (p<0.001). CONCLUSIONS: During inhibition of NF-KB, c-Jun Kinase levels remained unchanged. But no increase in cell death or necrosis was seen in tissue samples. Antiapoptotic effects were unchanged with the down-regulation of NF-KB. Minimal expression of NF-KB may be enough to protect against apoptosis in reperfusion injury.
    [Abstract] [Full Text] [Related] [New Search]