论文部分内容阅读
AIM:To investigate the role of nuclear factor kappa B(NF-κB) in the pathogenesis of lung injury induced byintestinal ischemia/reperfusion (I/R),and its effect onintercellular adhesion molecule-1 (ICAM-1) expressionand neutrophil infiltration.METHODS:Twenty-four Wistar rats weredivided randomly into control,I/R and pyrrolidinedithiocarbamate (PDTC) treatment groups,n=8 ineach.I/R group and PDTC treatment group receivedsuperior mysenteric artery (SMA) occluding for 1 h andreperfusion for 2 h.PDTC group was administrated withintraperitoneal injection of 2% 100 mg/kg PDTC 1 hbefore surgery.Lung histology and bronchia alveoluslung fluid (BALF) protein were assayed.Serum IL-6,lungmalondialdehyde (MDA) and myeloperoxidase (MPO) aswell as the expression level of NF-κB and ICAM-1 weremeasured.RESULTS:Lung injury induced by intestinal I/R,wascharacterized by edema,hemorrhage and neutrophilinfiltration as well as by the significant rising of BALFprotein.Compared to control group,the levels of serumIL-6 and lung MDA and MPO increased significantly in I/Rgroup (P=0.001).Strong positive expression of NF-κBp65 and ICAM-1 was observed.After the administrationof PDTC,the level of serum IL-6,lung MDA and MPOas well as NF-κB and ICAM-1 decreased significantly(P<0.05) when compared to I/R group. CONCLUSION:The activation of NF-kB plays animportant role in the pathogenesis of lung injury inducedby intestinal I/R through upregulating the neutrophilinfiltration and lung ICAM-1 expression.PDTC as aninhibitor of NF-kB can prevent lung injury induced byintestinal I/R through inhibiting the activity of NF-kB.
AIM: To investigate the role of nuclear factor kappa B (NF-κB) in the pathogenesis of lung injury induced by intestinal ischemia / reperfusion (I / R), and its effect onintercellular adhesion molecule-1 (ICAM-1) expression and neutrophil infiltration. METHODS: Twenty-four Wistar rats were divided into control, I / R and pyrrolidinedithiocarbamate (PDTC) treatment groups, n = 8 ineach.I / R group and PDTC treatment group received superior mysenteric artery (SMA) occluding for 1 h and reperfusion for 2 h .PDTC group was administrated with intraperitoneal injection of 2% 100 mg / kg PDTC 1 hbefore surgery. Lung histology and bronchia alveolus fluid (BALF) protein were assayed. Serum IL-6, lungmalondialdehyde (MDA) and myeloperoxidase (MPO) aswell as the expression levels of NF-κB and ICAM-1 were measured. RESULTS: Lung injury induced by intestinal I / R, was characterized by edema, hemorrhage and neutrophilin filtration as well as by the significant rising of BALF protein. Compared to control group, the levels of s The positive expression of NF-κBp65 and ICAM-1 was observed. After the administration of PDTC, the level of serum IL-6, lung MDA and MPO increased significantly in I / Rgroup (P = 0.001) CONCLUSION: The activation of NF-kB plays an important role in the pathogenesis of lung injury induced by intestinal I / R through upregulating the expression of NF-κB and ICAM-1 decreased significantly (P <0.05) when compared to I / R group. neutrophilinfiltration and lung ICAM-1 expression.PDTC as aninhibitor of NF-kB can prevent lung injury induced byintestinal I / R through inhibiting the activity of NF-kB.