Lipopolysaccharide from Escherichia coli prevents indomethacin-induced gastric damage in rats: role of non-protein sulfhydryl groups and leukocyte adherence

2009 ◽  
Vol 58 (10) ◽  
pp. 717-723 ◽  
Author(s):  
Antoniella Souza Gomes ◽  
Henrique Paula Lemos ◽  
Jand Venes Rolim Medeiros ◽  
Fernando Queiroz Cunha ◽  
Marcellus Henrique Loiola Ponte Souza
2006 ◽  
Vol 52 (1) ◽  
pp. 119-125 ◽  
Author(s):  
José Maurício S. C. Mota ◽  
Pedro M. G. Soares ◽  
Álvaro A. J. Menezes ◽  
Henrique P. Lemos ◽  
Fernando Q. Cunha ◽  
...  

2020 ◽  
Vol 327 ◽  
pp. 109166
Author(s):  
Thaise Boeing ◽  
Luisa Natália Bolda Mariano ◽  
Ana Caroline dos Santos ◽  
Bianca Tolentino ◽  
Angela Cadorin Vargas ◽  
...  

1997 ◽  
Vol 408-409 ◽  
pp. 177-180 ◽  
Author(s):  
Marianna Török ◽  
Kálmán Hideg ◽  
László Dux ◽  
LászlóI. Horváth

1997 ◽  
Vol 273 (6) ◽  
pp. G1246-G1251 ◽  
Author(s):  
John L. Wallace ◽  
Webb McKnight ◽  
Tammy L. Wilson ◽  
Piero Del Soldato ◽  
Giuseppe Cirino

The gastric damage associated with hemorrhagic shock appears to occur, at least in part, through neutrophil-dependent mechanisms. Nitric oxide (NO)-releasing derivatives of aspirin have been shown to spare the gastrointestinal tract of injury. As NO can inhibit neutrophil adherence, it is possible that such a derivative of aspirin (NCX-4016) would exert inhibitory effects on neutrophil adherence and therefore be capable of protecting the stomach against shock-induced gastric damage. This hypothesis was tested in this study. Oral administration of NCX-4016 or glyceryl trinitrate or depletion of circulating neutrophils with antineutrophil serum significantly reduced the extent of gastric damage induced by hemorrhagic shock, whereas aspirin had no effect. NCX-4016 and antineutrophil serum pretreatment resulted in significant preservation of gastric blood flow during the shock period. Moreover, NCX-4016, but not aspirin, was capable of inhibiting N-formyl-Met-Leu-Phe-induced leukocyte adherence to postcapillary mesenteric venules. These results suggest that an NO-releasing aspirin derivative reduces the susceptibility of the stomach to shock-induced damage through inhibitory effects on neutrophil adherence to the vascular endothelium.


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