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At least 163 records · Page 9Linked to original sources
PubMed2002

Effects of anti-inflammatory drugs and preservatives on morphologic characteristics and migration of canine corneal epithelial cells in tissue culture.

OBJECTIVE: To determine the effects of commonly used ophthalmic corticosteroids, suprofen, polysulfated glycosaminoglycan and preservatives on morphologic characteristics and migration of canine corneal epithelium grown in cell culture. ANIMALS STUDIED: Corneal epithelial cells harvested from the corneas of euthanized dogs were propagated in cell culture. PROCEDURES: Canine corneal epithelium was grown in tissue culture. The cells were treated with different corticosteroids, polysulfated glycosaminoglycan, suprofen or preservatives at different concentrations after a defect was created in the monolayer. Cellular morphologic characteristics and closure of the defect were compared between test drugs and controls. RESULTS: Morphologically the cells treated with dexamethasone were essentially the same as controls. Prednisolone and hydrocortisone caused rounding and shrinkage of the cells. Both suprofen and polysulfated glycosaminoglycan caused no apparent changes in morphologic characteristics at the lowest concentrations tested, but at higher concentrations there was a concentration-dependent degree of rounding and shrinkage. Benzylkonium chloride and thimerosal caused rounding and shrinkage of all the cells at all concentrations tested. Dexamethasone, hydrocortisone, and suprofen did not inhibit epithelial migration over the defects at the lowest concentrations tested. All other drugs and concentrations inhibited cellular migration. CONCLUSION: Dexamethasone affected the morphologic characteristics and migration of corneal epithelial cells less than hydrocortisone and prednisolone; therefore, dexamethasone may be the drug of choice when a corticosteroid is indicated and an epithelial defect is present. Suprofen and polysulfated glycosaminoglycan caused a concentration-dependent effect on morphologic characteristics and migration. The preservatives caused severe changes and inhibited migration of the canine corneal epithelial cells at all concentrations and may therefore contribute to poor epithelialization of ulcers treated with preservative-containing drugs.

Administration, Topical↗
PubMed1981

Synthesis of selectively 3H or 14C-labeled 2-(4-(2-thienylcarbonyl)phenyl)propionic acid.

2-(4-(2-Thienylcarbonyl)phenyl)propionic acid (suprofen), an anti-inflammatory agent, was labeled with tritium or carbon-14 for the purpose of investigating its metabolic fate in animals. The selectively tritiated suprofen (26.3-32.1 GBq (710-867 mCi)/mmol) was obtained by catalytic dehalogenation of the brominated precursor with 185-370 GBq (5-10 Ci) of tritium gas. The labeled position of the suprofen was confirmed by spectral data of the deuterated suprofen similarly synthesized. On the other hand, suprofen-14C (48.8 MBq (1.4 mCi)/mmol) was obtained by five-step synthesis from toluene [methyl-14C] in a 19% yield.

Anti-Inflammatory Agents↗
PubMed1981

Synthesis of optically active 2-(4-(2-thienylcarbonyl)-phenyl)propionic acid labeled with deuterium.

2-(4-(2-Thienylcarbonyl)phenyl)propionic acid (suprofen), an anti-inflammatory agent, was labeled with multiple-deuterium for the purpose of investigating the metabolism in man and animals by the ion cluster technique. Racemic suprofen-d4 was prepared by ten-stop synthesis from bromobenzene-d5 in a 32% yield, and its deuterium content was 99 atom%. This racemic suprofen-d4 was resolved by use of an optically active alpha-methylbenzylamine, resulting that optically active suprofen-d4 was obtained in a 11% yield and was 96.5 atom% D. On the other hand, suprofen-d7 (99 atom% D) was obtained by five-step synthesis from toulene-d8 and methyl-d3 iodide in a 24% yield.

Anti-Inflammatory Agents↗
PubMed1986

Effect of concurrent topical corticosteroid and NSAID therapy of experimental keratitis.

The ability of suprofen, a nonsteroidal anti-inflammatory drug, and prednisolone acetate, a corticosteroid, to suppress polymorphonuclear leukocyte invasion of the rabbit cornea during an experimental keratitis was evaluated following topical ophthalmic administration of either drug alone or both drugs concurrently. Suprofen therapy initiated immediately after induction of inflammation was ineffective. However, if suprofen therapy was begun 48 hr prior to the induction of inflammation, the drug was effective. In contrast, prednisolone acetate therapy begun after the induction of inflammation was effective; 48 hr of pretreatment with the corticosteroid produced a marked increase in its therapeutic effect. When administered according to the same regimen, concurrent therapy with suprofen and prednisolone acetate was significantly more effective than treatment with either drug alone. This result was obtained irrespective of whether concurrent therapy was initiated prior to or after the inflammatory event.

Administration, Topical↗
PubMed1992

Allosteric and competitive displacement of drugs from human serum albumin by octanoic acid, as revealed by high-performance liquid affinity chromatography, on a human serum albumin-based stationary phase.

A chiral stationary phase for high-performance liquid chromatography, based upon immobilized human serum albumin (HSA), was used to investigate the effect of octanoic acid on the simultaneous binding of a series of drugs to albumin. Octanoic acid was found to bind with high affinity to a primary binding site, which in turn induced an allosteric change in the region of drug binding Site II, resulting in the displacement of compounds binding there. Approximately 80% of the binding of suprofen and ketoprofen to HSA was accounted for by binding at Site II. Octanoic acid was found to also bind to a secondary site on HSA, with much lower affinity. This secondary site appeared to be the warfarin-azapropazone binding area (drug binding Site I), as both warfarin and phenylbutazone were displaced in a competitive manner by high levels of octanoic acid. The enantioselective binding to HSA exhibited by warfarin, suprofen and ketoprofen was found to be due to differential binding of the enantiomers at Site I; the primary binding site for suprofen and ketoprofen was not enantioselective.

Allosteric Site↗