Abstract
The objective of our work was to evaluate the effect of interferon-γ (IFN-γ) on cytokine expression in rat acute pancreatitis (AP). AP was introduced to rats which were divided into Control, AP and IFN-γ group. Rats in the AP and IFN-γ group were sacrificed as 6, 12 and 24 h after IFN-γ treatment. The serum amylase (AMA), endotoxin and cytokines were detected. The pathological examination and immunofluorescence staining of pancreas for TNF-α, NF-κB and IL-18 were performed. The serum AMA increased significantly at 6 h and reduced at 48 h after AP. The increase in IFN-γ was higher than that in AMA. IL-18 increased in the AP and IFN group, and IFN increased markedly at 48 h after AP. IL-27 reduced at 24 h after AP compared with AP group. In the AP group, the immunostaining of cytokines increased. In the IFN group, the edema in the pancreas was more severe, and NF-κB and IL-18 expression was higher than that in the other two groups. IFN-γ can increase serum IL-18 and reduce IL-27 in AP. IFN-γ can increase serum IL-18 and reduce serum IL-27 in AP. The increase in NF-κB and IL-18 may exert influence on pro-inflammatory cytokines to deteriorate inflammation in the pancreas. Thus, to control the IFN-γ might has promise to attenuate pancreatitis.
Highlights
Acute pancreatitis is a clinical entity that is believed to have intracellular activation of digestive enzymes and autodigestion of the pancreas as its central pathophysiologic cause [, ]
Acute pancreatitis (AP) is a common disease in clinical practice, and its pathogenesis is closely related to the abnormal activation of pancreatin, microcirculatory disturbance, reperfusion induced injury and release of inflammatory mediators and cytokines
AP was introduced to rats which were treated with interferon-γ (IFN-γ) and the cytokines were measured before and after treatment
Summary
Acute pancreatitis is a clinical entity that is believed to have intracellular activation of digestive enzymes and autodigestion of the pancreas as its central pathophysiologic cause [ , ]. As early as s and s, investigators felt that some mediators released during AP entered the systemic circulation, thereby causing dysfunction of distant organs [ ]. Efforts to unravel the events in the evolution of tissue damage in AP have shown a number of inflammatory mediators to be involved [ , ]. The proinflammatory response is countered by an anti-inflammatory response, and an imbalance between these two systems leads to localized tissue destruction and distant organ damage. Submitted: 7 December 2012 / Accepted: 9 February 2013 of the cascade leading to systemic inflammatory response syndrome and multiple organ dysfunction syndrome [ ]. Acute pancreatitis (AP) is a common disease in clinical practice, and its pathogenesis is closely related to the abnormal activation of pancreatin, microcirculatory disturbance, reperfusion induced injury and release of inflammatory mediators and cytokines.
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