Adhesion of carboxylate cements to hydroxyapatite. I. The effect of the structure of aliphatic carboxylates on their uptake by hydroxyapatite.
An investigation was made into the effect of the structure and functionality of aliphatic carboxylates on their sorption onto hydroxyapatite with a view to ascertaining factors affecting the adhesion of polyacrylate cements to tooth materials. In general, the amount of carboxylate sorbed was found to increase with the number of groups contained in the molecule. Thus, polyacrylate was found to be much more strongly sorbed than low molecular weight species. Sorption of the low molecular weight species appeared to be related to stereochemical factors rather than to the stability constants of their calcium chelates.
Adhesion of carboxylate cements to hydroxyapatite. II. Adsorption of aromatic carboxylates.
An investigation was made into the effect of structure and functionality of aromatic carboxylates on their adsorption on to hydroxyapatite (HAP) with a view to identifying factors affecting the adhesion of polyacrylate cements to tooth materials. In general, the amount of carboxylate adsorbed was found to increase with the number of groups contained in the molecule. The arrangement of these groups around the benzene ring also affected adsorption. These results suggested that adsorption was the result of a cooperative effect between carboxylate groups. An adsorption isotherm for mellitate on to HAP was constructed.
Protective effect of ginsenoside Re on acute gastric mucosal lesion induced by compound 48/80
The protective effect of ginsenoside Re, isolated from ginseng berry, against acute gastric mucosal lesions was examined in rats with a single intraperitoneal injection of compound 48/80 (C48/80). Ginsenoside Re (20 mg/kg or 100 mg/kg) was orally administered 0.5 h prior to C48/80 treatment. Ginsenoside Re dose-dependently prevented gastric mucosal lesion development 3 h after C48/80 treatment. Increases in the activities of myeloperoxidase (MPO; an index of neutrophil infiltration) and xanthine oxidase (XO) and the content of thiobarbituric acid reactive substances (TBARS; an index of lipid peroxidation) and decreases in the contents of hexosamine (a marker of gastric mucus) and adherent mucus, which occurred in gastric mucosal tissues after C48/80 treatment, were significantly attenuated by ginsenoside Re. The elevation of Bax expression and the decrease in Bcl2 expression after C48/80 treatment were also attenuated by ginsenoside Re. Ginsenoside Re significantly attenuated all these changes 3 h after C48/80 treatment. These results indicate that orally administered ginsenoside Re protects against C48/80-induced acute gastric mucosal lesions in rats, possibly through its stimulatory action on gastric mucus synthesis and secretion, its inhibitory action on neutrophil infiltration, and enhanced lipid peroxidation in the gastric mucosal tissue.