Colonization of gastric tissue in humans by H. pylori Gram-negative bacteria initiates gastric and duodenal ulcers and even gastric cancers. Infections promote inflammation and damage to gastric epithelium which might be followed by the impairment of its barrier function. The role of H. pylori components in these processes has not been specified. H. pylori cytotoxicity may potentially increase in the milieu of anti-inflammatory drugs including acetylsalicylic acid (ASA). The lipid transport-associated molecule such as low density lipoprotein (LDL), which is a classic risk factor of coronary heart disease (CHD) and 7-ketocholesterol (7-kCh) a product of cholesterol oxidation, which may occur during the oxidative stress in LDL could also be considered as pro-inflammatory. The aim of this study was to evaluate the cytotoxicity of H. pylori antigens, ASA, LDL and 7-kCh towards Kato III gastric epithelial cells, on the basis of the cell ability to reduce tetrazolium salt (MTT) and morphology of cell nuclei assessed by 4',6-diamidino-2-phenylindole (DAPI) staining. Kato III cells were stimulated for 24 h, at 37°C and 5% CO2, with H. pylori antigens: cytotoxin associated gene A (CagA) protein, the urease A subunit (UreA), lipopolysaccharide (LPS) and ASA, LDL or 7-kCh. H. pylori LPS, ASA, LDL and 7-kCh, but not H. pylori glycine acid extract (GE), demonstrated cytotoxicity against Kato III cells, which was related to a diminished percentage of MTT reducing cells and to an increased cell population with the signs of DNA damage. The results suggest that damage to gastric epithelial cells can be induced independently by H. pylori antigens, ASA and endogenous lipid transport-associated molecules. During H. pylori infection in vivo, especially in CHD patients, synergistic or antagonistic interactions between these factors might possibly influence the disease course. Further study is necessary to explain these potential effects.
The influence of a balanced diet (21 g% protein, 34 g% fat, 45 g% carbohydrate) with an isocaloric addition of non-oxidised or oxidised rapeseed oil, with and without garlic, on the development of hypercholesterolaemia was examined in 18 adult male rabbits divided into 3 equal groups. The rabbits from group 1 were fed fresh rapeseed oil, group II - received oxidised rapeseed oil, and group III - was given oxidised rapeseed oil and garlic. The concentration of 7-ketocholesterol and malondialdehyde (MDA) in plasma and free fatty acids (FAME) in blood serum was determined. The experiment lasted 24 weeks. At the beginning, and every six weeks, the rabbits were weighed and blood was taken. After the experiment was completed, the aorta was dissected for histological examinations. It was found that oxidised rapeseed oil caused an increase in the concentration of 7-ketocholesterol and FAME at the end of the experiment. MDA concentration increased in the 6th week of the experiment but did not appreciably change at the end of it. The obtained results suggested that the diet caused the development of hypercholesterolaemic alterations in the aorta wall and increased temporarily the level of 7-ketocholesterol, FAME, and MDA. Diet rich in oxidised oil modified significantly homeostasis of lipids in plasma and blood serum. The administration of garlic in such a diet inhibited atherosclerotic changes in the aorta wall and this seemed to be related to the decreasing concentration of 7-ketocholesterol and MDA in plasma and FAME in blood serum.
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