dinoprost and Corneal-Diseases

Deleterious effects of isopropyl unoprostone (PG-F2 alpha) on the ocular surface were evaluated using the in vivo barrier function assay of corneal epithelial cells and the proliferation assay of human corneal epithelial cells in vitro. The barrier function of corneal epithelial cells in vivo was not impaired by treatment with PGF2 alpha, but it was significantly suppressed by timolol. The result of cell proliferation assay of human corneal cells showed that the 0.12% PGF2 alpha ophthalmic solution caused greater suppression of cell proliferation and acuter cell toxicity than 0.5% timolol ophthalmic solution. Further study showed that not the vehicle but the PGF2 alpha itself was responsible for these deleterious effects. We conclude that the 0.12% PGF2 alpha ophthalmic solution affects cell migration and proliferation but not the barrier effects of the ocular surface. These results suggest that the corneal epithelial defect of glaucoma patients may be caused by these two independent mechanisms, namely suppression of cell proliferation by PGF2 alpha and the destruction of the barrier function of the ocular surface by timolol.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Cell Division; Cells, Cultured; Corneal Diseases; Dinoprost; Epithelium, Corneal; Female; Humans; Male; Middle Aged; Ophthalmic Solutions; Timolol

The involvement of prostaglandins (PGs) in the development of anterior segment ischaemia after occlusion of the bilateral long posterior ciliary arteries was investigated in rabbit eyes. In this experimental ischaemia, the tissue weight and protein content in the peripheral cornea and the protein content in the aqueous humour increased on the first postoperative day. Topically applied cyclooxygenase inhibitor diclofenac (0.1%) reduced corneal inflammation and further suppressed the elevation in the tissue weight and protein content in the peripheral cornea on day 1 after ischaemia, but did not affect the changes in the aqueous humour. Subconjunctivally administered PGE1 and PGE2 induced corneal oedema and increased corneal protein content in diclofenac-treated and ischaemia-induced eyes, but PGD2, PGF2alpha, and the stable PGI2 analogue cicaprost did not evoke any change. In fact, PGE2 content was markedly increased in the aqueous humour on day 1 after ischaemia, and diclofenac suppressed the increase. In addition, CPT-cAMP increased the corneal tissue weight and protein content in organ culture. These observations suggest that PGE2 may play an important role in developing corneal oedema at the initial stage of ischaemic damage, possibly through the cAMP-mediated pathway.

Topics: Alprostadil; Animals; Anterior Eye Segment; Aqueous Humor; Cornea; Corneal Diseases; Corneal Edema; Cyclic AMP; Cyclooxygenase Inhibitors; Diclofenac; Dinoprost; Dinoprostone; Ischemia; Male; Organ Culture Techniques; Prostaglandins; Proteins; Rabbits