Browsing by Subject "Indomethacin"

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    Effects of indomethacin on sunburn and suntan reactions in hairless descendants of Mexican hairless dogs
    (Murcia : F. Hernández, 1998) Kimura, T.; Doi, K.
    The inhibitory effects of topical indomethacin (1M)-treatment on sunburn and suntan reactions after ultraviolet (UV)-irradiation were investigated in the dorsal skin of hairless descendants of Mexican hairless dogs. Skin color, plasma prostaglandin E2 (PGE2) and histological features were examined. At 1 day after UV-irradiation, the IM-untreated sites showed prominent erythema, while the IM-treated sites exhibited few visible erythematous reactions. From 4 days after UV-irradiation, both the IM-treated and -untreated sites began to develop skin pigmentation. Assessment of skin color changes, using a colorimeter, reflected precisely the color changes in visual sunburn and suntan reactions. Plasma PGE2 concentration began to increase from 2 hours after UV-irradiation, reached the maximal values at 24 hours and recovered at 96 hours after UVirradiation. Histologically, at 1 day after UV-irradiation, the IM-untreated sites showed remarkable epidermal degeneration (thickening and sunburn cells) and moderate alteration in the dermis. On the other hand, the IM-treated sites showed only minor histological changes. At 4 days after UV-irradiation, deposition of melanin granules was found in both the IM-treated and -untreated sites. At 7 days after UV-irradiation, pigmentation became more prominent in the stratum basale. These results revealed that UV-induced erythematous reactions of hairless dogs were closely related to the action of PGE2. Visually and histologically, topical IMtreatment had apparent inhibitory effects on erythematous reactions, while this agent showed no protective effects on epidermal pigmentation after UV-irradiation.
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    Non-steroidal anti-inflammatory drugs (NSAIDs) and ovulation, lessons from morphology
    (Murcia : F. Hernández, 2006) Gaytán, M.; Morales, C.; Bellido, C.; Sánchez-Criado, J.E.; Gaytán, F.
    Ovulation constitutes the central event in ovarian physiology, and ovulatory disfunction is a relevant cause of female infertility. Non-steroidal antiinflammatory drugs (NSAIDs), widely used due to their analgesic and anti-inflammatory properties, consistently inhibit ovulation in all mammalian species investigated so far, likely due to the inhibition of cyclooxygenase 2 (COX-2), the inducible isoform of COX, that is the ratelimiting enzyme in prostaglandin (PG) synthesis. COX-2 inhibition has major effects on ovulation, fertilization and implantation, and NSAID therapy is likely implicated in human infertility and could be an important, frequently overlooked, cause of ovulatory disfunction in women. Although there is compelling evidence for a role of PGs in ovulation, the molecular targets and the precise role of these compounds in the ovulatory process are not fully understood. Morphological studies from rats treated with indomethacin (INDO), a potent inhibitor of PG synthesis, provide evidence on the actions of NSAIDs in ovulation, as well as on the posible roles of PGs in the ovulatory process. Cycling rats treated with INDO during the preovulatory period show abnormal ovulation, due to disruption of the spatial targeting of follicle rupture at the apex. Noticeably, gonadotropinprimed immature rats (widely used as a model for the study of ovulation) show age-dependent ovulatory defects similar to those of cycling rats treated with INDO. These data suggest that NSAID treatment disrupts physiological mechanisms underlying spatial targeting of follicle rupture at the apex, which are not fully established in very young rats. We summarize herein the ovulatory defects after pharmacologic COX-2 inhibition, and discuss the posible mechanisms underlying the anti-ovulatory actions of NSAIDs.