Sulfo-LewisxDiminishes Neutrophil Infiltration and Free Radicals with Minimal Effect on Serum Cytokines after Liver Ischemia and Reperfusion

García-Criado, Francisco Javier; Palma-Vargas, Juan; Valdunciel-Garcia, J. J.; Gómez‐Alonso, Alberto; Srivastava, O. P.; Ezrin, A.; Anderson, Mark; Toledo‐Pereyra, Luis H.

doi:10.1006/jsre.1997.5122

Cited by 14 publications

(10 citation statements)

References 24 publications

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“…* * * pϽ0.001 significantly different from time 0. Criado et al 17) reported that plasma TNF a and IL-1 level were significantly increased on the ischemia-reperfusion model. So we examined whether they have an influence on indomethacin induced gastric mucosal injury.…”

Section: Fig 4 Il-1 and Tnf A Concentration In Moouse Serum After Imentioning

confidence: 99%

Mechanism of Superoxide Generation System in Indomethacin-Induced Gastric Mucosal Injury in Rats.

Tanaka¹,

Yuda²,

Yamakawa

2001

Biological & Pharmaceutical Bulletin

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Indomethacin and several other nonsteroidal anti-inflammatory drugs (NSAID) are known to produce gastric mucosal injury.1,2) The pathogenesis of NSAID-induced gastric mucosal injury is reported for inhibition of prostaglandin (PG) biosynthesis 3) and depletion of gastric mucosal blood flow. 4,5) A number of studies have highlighted the importance of alterations in mucosal blood flow after NSAID administration. By this depletion of gastric mucosal blood flow, polymorphonuclear leukocytes (PMN) were infiltlated to gastric mucosal tissue. 6) We clarified these phenomena that PMN infiltlates, generates oxygen radicals and induces direct gastric mucosal injury, and then increasing lipid peroxidation further aggravate damage in previous study. 7) We demonstrated that neutrophil-derived free radicals are also important factors in the gastric mucosal injury induced ischemia-reperfusion in pylorus-ligated rats.8) But the generation system of oxygen free radicals is not clear in the indomethacin induced-gastric mucosal injury. We examined this and report here the mechanism of pathogenesis in this type of injury.Superoxide radicals have several generation systems, with activation of xanthine-xanthine oxidase (XOD) enzyme in vein cellular tissue and activation of NADPH oxidase enzyme in PMN being the main ones. The direct effect of indomethacin on XOD activity in vitro and NADPH oxidase in ex vivo was therefore examined.Cytokines, IL-1 and TNF a are well known to play important roles in inflammation.9) The first step of PMN infiltration into an inflammation site is believed to take place in many cytokines and the growth binding factors IL-1 and TNF a from mast cells and macrophages. We measured cytokines to learn whether indomethacin acts to directly activate the oxygen radical generation system or is a second any effect. MATERIALS AND METHODS AnimalsMale Donryu rats (SPF) 8 weeks old were obtained from Charles River Co., Tokyo, and ICR mice (SPF) 8 weeks old were obtained from SLC Japan Co., Tokyo.Materials Indomethacin, ferricytochrome C (horse heart type III), NADPH Na (type III), NBT and BCIP were obtained from Sigma, and xanthine oxidase solution from Boehringer Mannheim Yamanouchi, Tokyo. Diphenylene iodonium chloride was from ALEXIS Co., U.S.A.; Bio-Rad protein assay was from BIO RAD; anti p47 phox was from Trunsduction Laboratories and mouse IL-1 and the TNF a assay system were obtained from Genzyme. Other chemicals were of reagent grade and were used without purification.Assay of Xanthine Oxidase (XOD) Activity XOD reduced cytochrome c was monitored spectrophotometrically at 550 nm. The reaction mixture consisted of 100 mM potassium phosphate buffer (pH 7.4) (1.2 ml), 0.1 mM cytochrome c (0.2 ml), 5 mM xanthine (0.2 ml) and 0.1 U/ml xanthine oxidase solution (0.2 ml). This mixture was preincubated for 5 min at 37°C and indomethacin was added at a fianl concentration of 0.1, 0.5, 1, 5, or 10 mM. Indomethacin was disorbed by 100% ethanol solution and finally diluted with distilled water at Ͻ1% ethanol concentration.G...

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Section: Fig 4 Il-1 and Tnf A Concentration In Moouse Serum After Imentioning

confidence: 99%

Mechanism of Superoxide Generation System in Indomethacin-Induced Gastric Mucosal Injury in Rats.

Tanaka¹,

Yuda²,

Yamakawa

2001

Biological & Pharmaceutical Bulletin

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“…In a previous study, our group [35] tested the drug used here for the first time, in vivo, in a hepatic ischemia-reperfusion model.…”

Section: Discussionmentioning

confidence: 99%

P- and E-Selectin Blockade Can Control Bacterial Translocation and Modulate Systemic Inflammatory Response

García-Criado¹,

Lozano²,

Barros³

et al. 2005

Journal of Investigative Surgery

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Bacterial translocation is an important phenomenon in clinical medicine and leads to an increase in patient morbidity and mortality by multiple organ failure. The selectin family plays an important role in the pathogenesis of inflammation, causing an increase in leukocyte-endothelium interactions and inducing a greater leukocyte's migration. This study considered the effect of a sulfo derivative of Sialyl-Lewis(X), GM 1998-016, that will block the P- and E-selectins interaction with a ligand, the Sialyl-Lewis(X), valuing the modulation of the systemic inflammatory response and the induced translocation. Seventy-five Wistar male rats were injected intraperitoneally with Zymosan A and treated with different doses of GM 1998-016 according to study groups. Measurements of values of qualitative and quantitative microbiology, neutrophil infiltration (myeloperoxidase), oxygen free radicals (superoxide anion, superoxide dismutase, catalase, and gluthatione peroxidase), and cytokines (tumor necrosis factor-alpha and interleukin-1beta) were taken at different times after Zymosan administration. A significant decrease of bacterial translocation, both local (MLN) and systemic (p < .05), was observed, with a decrease in the neutrophil infiltration (p < .001), the oxygen free radicals production (p < .01) and the studied cytokines (p < .01). In conclusion, GM 1998-016 showed a protective effect in an in vivo experimental model of bacterial translocation, downregulating the inflammatory response and the leukocyte-endothelium interactions.

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“…[21][22][23] The function of CAT is to divide H 2 O 2 into O 2 and H 2 O by participating in the reaction with H 2 O 2 , thereby preventing the formation of OH radicals, which are more toxic. 24,25 N-Acetylcysteine has a mucolytic and antioxidant effect. It obtains oxygenation of tissues and can protect the spinal cord partially from reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Prevention of reperfusion injury of the spinal cord in aortic surgery: An experimental study

et al. 2008

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Sulfo-LewisxDiminishes Neutrophil Infiltration and Free Radicals with Minimal Effect on Serum Cytokines after Liver Ischemia and Reperfusion

Cited by 14 publications

References 24 publications

Mechanism of Superoxide Generation System in Indomethacin-Induced Gastric Mucosal Injury in Rats.

Mechanism of Superoxide Generation System in Indomethacin-Induced Gastric Mucosal Injury in Rats.

P- and E-Selectin Blockade Can Control Bacterial Translocation and Modulate Systemic Inflammatory Response

Prevention of reperfusion injury of the spinal cord in aortic surgery: An experimental study

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