ArticleWorld journal of gastroenterology2006
Effect of nuclear factor kappa B on intercellular adhesion molecule-1 expression and neutrophil infiltration in lung injury induced by intestinal ischemia/reperfusion in rats.
Article in World journal of gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 27 citations in OpenAlex.
- Curcumin (a constituent of turmeric): New treatment option against COVID-19.Food science & nutrition · 2020Review
- Anti-inflammatory and antioxidant effects of curcumin on acute lung injury in a rodent model of intestinal ischemia reperfusion by inhibiting the pathway of NF-Kb.International journal of clinical and experimental pathology · 2015Article
- Pathophysiological Approaches of Acute Respiratory Distress syndrome: Novel Bases for Study of Lung Injury.The open respiratory medicine journal · 2015Article
- Intestinal mucosal barrier is injured by BMP2/4 via activation of NF-κB signals after ischemic reperfusion.Mediators of inflammation · 2014Article
- The protective effects of curcumin on experimental acute liver lesion induced by intestinal ischemia-reperfusion through inhibiting the pathway of NF-κB in a rat model.Oxidative medicine and cellular longevity · 2014Article
- Suppressive effect of low-level laser therapy on tracheal hyperresponsiveness and lung inflammation in rat subjected to intestinal ischemia and reperfusion.Lasers in medical science · 2013Article
- Strategies for modulating the inflammatory response after decompression from abdominal compartment syndrome.Scandinavian journal of trauma, resuscitation and emergency medicine · 2012Review
- Protective effect of carnosol on lung injury induced by intestinal ischemia/reperfusion.Surgery today · 2010Article
- Preconditioning of isoflurane on spinal cord ischemia can increase the number of inducible nitric oxide synthase-expressing motor neurons in rat.Korean journal of anesthesiology · 2010Article
- Lung injury associated with bortezomib therapy in relapsed/refractory multiple myeloma in Japan: a questionnaire-based report from the "lung injury by bortezomib" joint committee of the Japanese society of hematology and the Japanese society of clinical hematology.International journal of hematology · 2006Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the role of nuclear factor kappa B (NF-kappaB) in the pathogenesis of lung injury induced by intestinal ischemia/reperfusion (I/R), and its effect on intercellular adhesion molecule-1 (ICAM-1) expression and neutrophil infiltration.
methodsTwenty-four Wistar rats were divided randomly into control, I/R and pyrrolidine dithiocarbamate (PDTC) treatment groups, n=8 in each. 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 h before surgery. Lung histology and bronchia alveolus lung fluid (BALF) protein were assayed. Serum IL-6, lung malondialdehyde (MDA) and myeloperoxidase (MPO) as well as the expression level of NF-kappaB and ICAM-1 were measured.
resultsLung injury induced by intestinal I/R, was characterized by edema, hemorrhage and neutrophil infiltration as well as by the significant rising of BALF protein. Compared to control group, the levels of serum IL-6 and lung MDA and MPO increased significantly in I/R group (P=0.001). Strong positive expression of NF-kappaB p65 and ICAM-1 was observed. After the administration of PDTC, the level of serum IL-6, lung MDA and MPO as well as NF-kappaB and ICAM-1 decreased significantly (P<0.05) when compared to I/R group.
conclusionThe activation of NF-kappaB plays an important role in the pathogenesis of lung injury induced by intestinal I/R through upregulating the neutrophil infiltration and lung ICAM-1 expression. PDTC as an inhibitor of NF-kappaB can prevent lung injury induced by intestinal I/R through inhibiting the activity of NF-kappaB.
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