World J Gastroentero
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World J Gastroentero · Nov 2003
Effect of NF-kappaB and p38 MAPK in activated monocytes/macrophages on pro-inflammatory cytokines of rats with acute pancreatitis.
Proinflammatory cytokines TNF-alpha and IL-6 play a main role in acute pancreatitis (AP). Cytokine biosynthesis runs through two major signaling pathways at the level of proteins: nuclear transcription factor-kappaB (NF-kappaB) and p38 mitogen-activated protein kinase (p38 MAPK). The aim of the study was to investigate the effect of NF-kappaB and p38 MAPK in activated monocytes/macrophages on cytokines of rats with acute pancreastitis. ⋯ Cytokine TNF-alpha and IL-6 play a main role in acute pancreatitis, expression of NF-kappaB and p38 MAPK in activated monocytes/macrophages might play a major role in cytokine transcription and biosynthesis.
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World J Gastroentero · Oct 2003
Effect of ischemic preconditioning on P-selectin expression in hepatocytes of rats with cirrhotic ischemia-reperfusion injury.
To investigate the effects and mechanisms of ischemic preconditioning (IPC) on the ischemia/reperfusion (I/R) injury of liver cirrhosis in rats and the effect of IPC on P-selectin expression in hepatocytes. ⋯ IPC can attenuate the damage induced by I/R in cirrhotic liver and increase the ischemic tolerance of the rats with liver cirrhosis. IPC can abolish I/R induced leukocyte adhesion and infiltration by preventing post-ischemic P-selectin expression in the rats with liver cirrhosis via a NO-initiated pathway.
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World J Gastroentero · Sep 2003
Clinical effects of continuous high volume hemofiltration on severe acute pancreatitis complicated with multiple organ dysfunction syndrome.
To investigate the efficiency of continuous high volume hemofiltration (HVHF) in the treatment of severe acute pancreatitis (SAP) complicated with multiple organ dysfunction syndrome (MODS). ⋯ HVHF is technically possible in SAP patients complicated with MODS. It does not appear to have detrimental effects and may have beneficial effects. Continuous HVHF, which seldom disturbs the hemodynamics and causes few side-effects, is expected to become a beneficial adjunct therapy for SAP complicated with MODS.
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World J Gastroentero · Jun 2003
Rapid mitogen-activated protein kinase by basic fibroblast growth factor in rat intestine after ischemia/reperfusion injury.
Previous studies showed that exogenous basic fibroblast growth factor (bFGF or FGF-2) could improve physiological dysfunction after intestinal ischemia/ reperfusion (I/R) injury. However, the mechanisms of this protective effect of bFGF are still unclear. The present study was to detect the effect of bFGF on the activities of mitogen-activated protein kinase (MAPK) signaling pathway in rat intestine after I/R injury, and to investigate the protective mechanisms of bFGF on intestinal ischemia injury. ⋯ The results indicate that intestinal I/R injury stimulates the activities of MAPK pathways, and that p42/p44 MAPK and p38MAPK activities are necessary for the protective effect of exogenous bFGF on intestinal I/R injury. The protective effect of bFGF on intestinal dysfunction may be mediated by the early activation of p42/p44 MAPK and p38 MAPK signaling pathways.
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World J Gastroentero · May 2003
Imbalance between expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in invasiveness and metastasis of human gastric carcinoma.
The expressive balance between matrix metalloproteinase-9 (MMP-9) and its tissue inhibitor of metalloproteinase-1 (TIMP-1) plays a critical role in maintaining the degradation and synthesis of extracellular matrix. Loss of such balance is associated with invasion and metastasis of tumors. This study aimed to determine the expression of MMP-9 and TIMP-1 in gastric carcinoma, and the association of the expressive imbalance between MMP-9 and TIMP-1 with the invasion and metastasis and prognosis of gastric carcinoma. ⋯ Our results in gastric carcinoma demonstrated a significant positive association of MMP-9 over-expression with proliferation of tumor cells, the depth of invasiveness, lymph node metastasis and TNM stage, suggesting MMP-9 can serve as a molecular marker of tumor invasion and metastasis. We also demonstrate a significant negative relationship of TIMP-1 expression with the depth of invasiveness and lymph node metastasis, which provide a new idea in the tumor biological and genetic treatment. The interaction between MMP-9 and TIMP-1 in the processes of tumor invasion and metastasis is that MMP-9 mainly promotes tumor invasion and metastasis and TIMP-1 inhibits functions of MMP-9. The imbalance between MMP-9 and TIMP-1 expression may suggest the occurrence of tumor invasion and metastasis, predict poor prognosis. For patients with imbalanced MMP-9 and TIMP-1 expression, the optimal treatment scheme needs to be selected.