ISSN:
1573-2568
Keywords:
ADAPTIVE CYTOPROTECTION
;
PROSTAGLANDINS
;
BILE SALTS
;
AGS CELLS
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract The majority of previous work investigatingadaptive cytoprotection has involved in vivo studies,which have suggested that this protective response is inlarge part mediated by endogenous prostaglandins (PGs). The aim of this study was to investigateadaptive cytoprotection under in vitro conditions inhuman gastric cells and to better delineate the role ofendogenous PGs in this protective response. AGS cells (a human gastric carcinoma cell line)were characterized morphologically and subsequently usedfor all experiments. Sodium deoxycholate was used asboth the mild irritant and the damaging agent, and cell injury was quantified using both acommercial viability/cytotoxicity kit as well astransepithelial permeability studies. Finally,endogenous PG synthesis in response to varyingconcentrations of deoxycholate was determined. AGS cells were determined to bemorphologically similar to gastric mucous cells.Pretreatment of cells with low-dose deoxycholatesignificantly attenuated injury upon subsequent exposure to damaging concentrations of deoxycholate, andthis protection was determined to be dependent upon bothconcentration and duration of mild irritant exposure.Preincubation of AGS cells with indomethacin reversed protection induced by mild irritantpretreatment and also significantly increased cellularsusceptibility to injury. Results of the permeabilitystudies closely paralleled those assessing cell mortality. While deoxycholate exposureincreased PG synthesis, the concentrations required weremuch higher than those needed to initiate protection.Adaptive cytoprotection exists in AGS cells under in vitro conditions independent of intact bloodflow, neural innervation, or circulating humoralmediators. While this protection is reversed byindomethacin, it appears that this reversal results fromincreased cellular injury secondary to diminished basalPGs, rather than inhibition of endogenous PGsynthesis.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1018826416864
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