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Histamine protects against the acute phase of experimentally-induced hepatic ischemia/re-perfusion.
- Source :
- Journal of Immunotoxicology; Jan-Mar2013, Vol. 10 Issue 1, p9-16, 8p, 1 Color Photograph, 6 Graphs
- Publication Year :
- 2013
-
Abstract
- Histamine, involved in many inflammatory reactions and immune responses, is reported to suppress-via H4R stimulation-injury concomitant with the late phase of warm hepatic ischemia/re-perfusion (I/R). The current study investigated the possible effects of histamine on the acute phase of hepatic I/R injury, and the possible underlying mechanisms like oxidative stress and release of inflammatory cytokines (e.g., tumor necrosis factor (TNF)-α nd interleukin [IL]-12). Rats were divided into naïve, sham-operated, and I/R groups. The I/R group was divided into sub-groups and pre-treated with histaminergic ligands before induction of ischemia. Anesthetized rats were subjected to warm ischemia for 30 min by occlusion of the portal vein and hepatic artery, then re-perfused for 90 min. Rats in the control I/R group showed significant increases in hepatic malondialdehyde (MDA), TNF α, and IL-12 contents, and in plasma alanine transaminase (ALT) and aspartate transaminase (AST) levels, along with significant decreases in hepatic reduced glutathione (GSH) content and marked diffuse histopathologic damage. Pre-treatment with histamine resulted in significant mitigation of each of these end-points. The protective effect of histamine was not antagonized by pre-treatment with mepyramine (H1R antagonist) or ranitidine (H2R antagonist) and completely reversed by pre-treatment with thioperamide (H3R and H4R antagonist). In addition, the histamine protective effect was mimicked by pre-treatment of rats with clozapine (H4R agonist). These observations strongly suggested that histamine has a protective effect against hepatic I/R-mediated tissue injury during the acute phase, and this effect was mediated through an H4R stimulation that led to a decrease in IL-12 and TNF α production-outcomes that consequently decreased localized oxidative stress and afforded hepatic protection in general. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 1547691X
- Volume :
- 10
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Journal of Immunotoxicology
- Publication Type :
- Academic Journal
- Accession number :
- 85716873
- Full Text :
- https://doi.org/10.3109/1547691X.2012.684158