The Pathophysiologic Role of Cyclooxygenases in the Eye

Radi, Smaail; Render, James A.

doi:10.1089/jop.2007.0078

Cited by 30 publications

(25 citation statements)

References 90 publications

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“…The COX-2 isoenzyme is not generally expressed in normal ocular tissues but is up-regulated during pathologic conditions (Table 5). COX-2 expression is increased with ocular inflammation or ocular injury (Radi and Render 2008).…”

Section: Cox-1 and Cox-2 Expression In The Eyementioning

confidence: 99%

Pathophysiology of Cyclooxygenase Inhibition in Animal Models

Radi

2009

Toxicol Pathol

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Cyclooxygenase (COX) catalyzes the conversion of arachidonic acid into prostaglandins (PGs), which play a significant role in health and disease in the gastrointestinal tract (GI) and in the renal, skeletal, and ocular systems. COX-1 is constitutively expressed and found in most normal tissues, whereas COX-2 can be expressed at low levels in normal tissues and is highly induced by pro-inflammatory mediators. Inhibitors of COX activity include: (1) conventional nonselective, nonsteroidal anti-inflammatory drugs (ns-NSAIDs) and (2) COX-2 selective nonsteroidal antiinflammatory drugs (COX-2 s-NSAIDs). Inhibition of COX-1 often elicits GI toxicity in animals and humans. Therefore, COX-2 s-NSAIDs were developed to provide a selective COX-2 agent, while minimizing the attendant COX-1-mediated GI toxicities. Rats and dogs overpredict COX inhibition for renal effects such as renal handling of electrolytes in humans. COX inhibitors are shown to have both beneficial and detrimental effects, such as on healing of ligament or tendon tears, on the skeletal system in animal models. Certain ophthalmic conditions such as glaucoma and keratitis are associated with increased COX-2 expression, suggesting a potential role in their pathophysiology.

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Section: Cox-1 and Cox-2 Expression In The Eyementioning

confidence: 99%

Pathophysiology of Cyclooxygenase Inhibition in Animal Models

Radi

2009

Toxicol Pathol

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“…This condition was most severe in the superior bulbar conjunctiva (the site of the device insertion), and persisted in some eyes (15%) until POD 60 (p = 0.07). We considered that device insertion was the most likely cause of this hyperemia because it has been shown to be associated with a high likelihood to cause inflammation (RADI & RENDER, 2008) and the conjunctiva was highly vascularized. However, it is important to mention that inflammation was not reported by FIALHO et al (2006) after device insertion.…”

Section: Resultsmentioning

confidence: 99%

Effect of an intravitreal dexamethasone device on ocular inflammation after phacoemulsification in dogs

et al. 2016

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This study examined the efficacy of an intravitreal dexamethasone-loaded device for the control of postoperative ocular inflammation in dogs following RESUMO O estudo examinou a eficácia de um dispositivo intravítreo de liberação de dexametasona para o controle da inflamação ocular em cães, após facoemulsificação. Um dispositivo de copolímero poli (ácido lático-co-glicólico) foi implantado via pars plana na câmera vítrea, imediatamente antes da facoemulsificação (grupo dispositivo [GD], n=20). Após a cirurgia, o grupo controle (GC) recebeu terapia esteroide, midriático e antibiótico. O mesmo protocolo de tratamento foi adotado no GD, exceto pelos esteroides. Todos os olhos foram examinados antes do procedimento e em diferentes tempos após a facoemulsificação. A ultrassonografia mostrou que o dispositivo diminuiu em tamanho, sendo observado, apenas, remanescentes aos 60 dias de pós-operatório (DPO). Sinais de uveíte foram observados em 35% do GD no DPO 7, entretanto, no DPO 14, 50% dos

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“…Inhibition of COX-2 activation and eicosanoids formation has been associated with attenuating angiogenesis and downregulating VEGF and bFGF [53]. The COX-2 isoenzyme is up-regulated during ocular inflammation or ocular injury [54]. Within the retina, the expression of COX-2 and VEGF, along with the production of prostaglandins, may be induced by hyperglycemia and tissue hypoxia while inhibition of COX-2 has been effective at reducing the production of VEGF, neovascularization and BRB leakage in relevant models of ocular diseases, suggesting a significant role of prostaglandins in pathological vascular leakage and angiogenesis [54,55,56].…”

Section: Discussionmentioning

confidence: 99%