Abstract
Hepatocellular dysfunction occurs early in sepsis and this appears to be caused by Kupffer cell-derived TNF-α production from the liver as a result of the increased release of the sympathetic neurotransmitter, norepinephrine, from the gut. Ghrelin, a novel stomach-derived peptide, is down-regulated in sepsis and administration of ghrelin into rodents decrease pro-inflammatory cytokines, attenuates hepatic and other organ injuries and improves survival. Ghrelin's beneficial effect in sepsis is mediated by the inhibition of the sympathetic nervous system (SNS), as evidenced by the reduced gut-derived norepineprine (NE) release in sepsis after ghrelin treatment. Recent data suggest that MKP-1, the MAPK phosphatase-1, is involved in the innate immune responses. To determine that the beneficial effect of ghrelin in sepsis is mediated by MKP-1, rats were subjected to sepsis by cecal ligation and puncture (CLP) alone, or treated with ghrelin, beginning at 5-h post-CLP and liver tissues were harvested and examined for MKP-1 mRNA and protein expression. CLP alone produced a significant decrease in MKP-1 gene expression in liver tissues at 20 h after CLP (P
Original language | English (US) |
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Pages (from-to) | 159-164 |
Number of pages | 6 |
Journal | International Journal of Molecular Medicine |
Volume | 25 |
Issue number | 1 |
DOIs | |
State | Published - 2010 |
Externally published | Yes |
Keywords
- Ghrelin
- Inflammation
- MAPK phosphatase-1
- Norepinephrine
- Sepsis
ASJC Scopus subject areas
- Genetics