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PubMedDate not supplied

Poly(4-vinylpyridine)-coated liposomes: stability studies and release of acetylsalicylic acid.

Liposomes of dimyristoylphosphatidylcholine (DMPC) and dicetylphosphate (DCP) reacted with 4-vinylpyridine (4-VP) to form a salt and, subsequently, autopolymerized for form poly(4-vinylpyridine) (poly(4-VP))-coated liposomes. The conditions for optimization of polymer coating have been determined; also, the effects of polymer coating on liposome stability, the encapsulation of ASA and its release kinetics have been measured. The coating efficiency was maximum at a DMPC:DCP 1:1 mole ratio, at pH 4.0 in acetate buffer, and a polymerization time of 40 min. The polymer-coated liposomes were stable in 2 mM sodium cholate and 4 per cent isopropanol solutions, as determined from turbidity measurements, versus a 20-25% decrease in stability of uncoated liposomes. The encapsulation efficiency of ASA reached a maximum of 9 per cent at DMPC:DCP 1:1 mole ratio. The release of ASA at 37 degrees C, pH 7.0 was characterized by an initial fast release (85 and 63 per cent in 20 min from uncoated and polymer-coated liposomes, respectively) followed by a slow, constant release rate up to 140 min. Thus, autopolymerization of a polymerizable monomer at liposome surfaces represents a potentially feasible stabilization approach for liposomes exposed to sodium cholate solutions with greater retention of solute than uncoated liposomes.

Aspirin↗
PubMed1981

A comparison of the effects of HP 549 (Isoxepac), indomethacin and acetylsalicylic acid (Aspirin) on gastric mucosa in man.

To determine the reaction of the gastric mucosa to HP 549 (isoxepac) an oxo-dibenz-oxepine derivative of acetic acid and new non-steroidal antiphlogistic agent in comparison with standard drugs, 12 healthy volunteers received 3 g of Aspirin, 150 mg of indomethacin, or 600 mg of HP 549 (isoxepac) in a double-blind cross-over trial. Before and after each treatment period, all subjects underwent gastroscopy with biopsy of gastric mucosa. The subjects recorded complaints (side effects) before and after each treatment period. Aspirin produced significantly more gross mucosal changes at endoscopy. There was no significant difference between isoxepac and indomethacin. Both produced very few gastric mucosal changes and there were few subjective complaints.

Acetates↗
PubMed2005

Effect of the ulcerogenic agents ethanol, acetylsalicylic acid and taurocholate on actin cytoskeleton and cell motility in cultured rat gastric mucosal cells.

AIM: To assess the effects of ulcerogenic agents on actin cytoskeleton and cell motility and the contribution of oxidative stress. METHODS: Rat gastric mucosal cell monolayers were cultured on coverslips. The cells were exposed, with or without allopurinol (2 mmol/L), for 15 min to ethanol (10-150 mL/L), ASA (1-20 mmol/L) or taurocholate (1-20 mmol/L), then the cells were processed for actin and vinculin staining. Cell migration after wounding was also measured. RESULTS: Exposure to 10 mL/L ethanol caused divergence of zonula adherens-associated actin bundles of adjacent cells and decreased rate of migration. These actions were opposed by xanthine oxidase inhibitor allopurinol. Exposure to 50 mL/L ethanol induced degradation and divergence of zonula adherens-associated vinculin from adjacent cells, which was, again, partially reverted by allopurinol. With 1 mmol/L ASA actin filaments became shorter and thicker. However, higher concentrations (10, 20 mmol/L) of ASA returned microfilaments thinner and longer, and decreased rate of migration. Zonula adherens-associated actin bundles were moderately distorted with 10 mmol/L ASA and with 10 mmol/L taurocholate. Exposure to taurocholate provoked changes resembling those of ASA. Taurocholate 5-20 mmol/L decreased the rate of migration dose dependently. The effects of ASA and taurocholate were not prevented by allopurinol. CONCLUSION: All ulcerogenic agents decreased the rate of migration dose dependently and induced divergence of zonula adherens-associated actin bundles of adjacent cells. In addition, ethanol and ASA caused degradation of actin cytoskeleton. Oxidative stress seems to underlie ethanol, but not ASA or taurocholate, induced cytoskeletal damage.

Actins↗
PubMed1983

Chemical feasibility studies concerning potential prodrugs of acetylsalicylic acid.

A rationale is developed for aspirin prodrugs based on non-acidic latentiated derivatives. Knowledge of the gastro-intestinal liabilities and pharmacological profile is required for this approach whereby aspirin is built into a common ortho ester function of the type 2-substituted 2-methyl-4H-1,3-benzodioxin-4-one with latentiated carboxyl and acetoxy groups. Twelve compounds of this type, ten substituted with various alkoxy and aryloxy groups and two with arylthio groups, have been isolated and characterized. A new synthetic route, comprising the reaction of 2-acetoxybenzoyl chloride with TMS derivatives of the corresponding alcohols and phenols, has been devised for the preparation of some of the compounds while others were prepared according to known methods. Subsequently, the prodrug candidates have been subjected to non-enzymatic hydrolysis for a first rapid screening in vitro. Only 2-tert-butoxy-2-methyl-4H-1,3-benzodioxin-4-one is observed to act as a true proaspirin, releasing aspirin, under these conditions, but analogous compounds with tertiary substituents may display the same behavior, and this chemical approach to aspirin modification may offer a viable rationale for aspirin prodrugs with reduced gastric irritancy or for making "superaspirins".

Aspirin↗