ocular hypertension/hypoxia

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microRNA-320a prevent Müller cells from hypoxia injury by targeting aquaporin-4

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Müller cells are closely related to diabetic retinopathy (DR). Aquaporin-4 (AQP4) can effectively promote the diffusion of water across cellular membranes. However, the dynamic balance of water plays key role in many diseases, such as cerebral edema. Meanwhile, the unusual expression and

HIF‑1 signaling pathway involving iNOS, COX‑2 and caspase‑9 mediates the neuroprotection provided by erythropoietin in the retina of chronic ocular hypertension rats.

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This study aimed to investigate the impacts of erythropoietin (EPO) on the electroretinogram b‑wave (ERG‑b), and on the mRNA and protein expression levels of hypoxia‑inducible factor‑1α (HIF‑1α), inducible nitric oxide synthase (iNOS), cyclooxygenase‑2 (COX‑2) and caspase‑9 in chronic ocular

Increased Antioxidant Capacity and Pro-Homeostatic Lipid Mediators in Ocular Hypertension-A Human Experimental Model

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The main risk factor for primary open-angle glaucoma (POAG) is increased intraocular pressure (IOP). It is of interest that about half of the patients have an IOP within the normal range (normal-tension glaucoma, NTG). Additionally, there is a group of patients with a high IOP but no glaucomatous

Investigations into Hypoxia and Oxidative Stress at the Optic Nerve Head in a Rat Model of Glaucoma.

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The vascular hypothesis of glaucoma proposes that retinal ganglion cell axons traversing the optic nerve head (ONH) undergo oxygen and nutrient insufficiency as a result of compromised local blood flow, ultimately leading to their degeneration. To date, evidence for the hypothesis is largely

Inflammasome Activation Induces Pyroptosis in the Retina Exposed to Ocular Hypertension Injury.

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Mechanical stress and hypoxia during episodes of ocular hypertension (OHT) trigger glial activation and neuroinflammation in the retina. Glial activation and release of pro-inflammatory cytokines TNFα and IL-1β, complement, and other danger factors was shown to facilitate injury and loss of retinal

Evidence of Hypoxic Glial Cells in a Model of Ocular Hypertension.

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Reoxygenation after hypoxia can increase reactive oxygen species and upregulate autophagy. We determined, for the first time, the impact of elevated IOP on hypoxia induction, superoxide accumulation, and autophagy in a bead model of glaucoma.Ocular

Up-regulated endogenous erythropoietin/erythropoietin receptor system and exogenous erythropoietin rescue retinal ganglion cells after chronic ocular hypertension.

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OBJECTIVE Recent studies have showed that erythropoietin (EPO) is a neuroprotectant for central nerve system neurons in addition to being a hematopoietic cytokine in response to hypoxia. In this study, we investigate the role of the EPO/EPO receptor (EPOR) system in the rat retina after ocular

Postural studies in pulsatile ocular blood flow: I. Ocular hypertension and normotension.

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Measurements of pulsatile ocular blood flow (POBF) have been recorded in a group of healthy, ocular normotensive volunteers and ocular hypertensive patients recruited from outpatients. Use of a pneumotonometric probe linked to a Langham ocular blood flow system enabled readings of intraocular

Electro-oculogram changes in patients with ocular hypertension and primary open-angle glaucoma.

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Recent evidence suggests that retinal hypoxia and ischemia affect the standing potential of the eye and the activity of the photoreceptors. To test whether chronically elevated intraocular pressure would produce similar effects, we measured electro-oculograms in two groups of patients: ocular

Rapid resolution of venous stasis retinopathy after carotid endarterectomy.

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A 60-year-old woman with ocular hypertension developed unilateral venous stasis retinopathy and neovascularization of the optic disk as the first signs of carotid occlusive disease. The retinopathy and the neovascularization disappeared rapidly and dramatically after carotid endarterectomy.

Interaction between nalbuphine and alfentanil on intraocular pressure and pupil size of conscious rabbits.

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The ocular hypertension caused by the mu agonist alfentanil (10 micrograms/kg, i.v.) in spontaneously breathing rabbits was reversed to ocular hypotension by pretreatment with the kappa agonist-mu antagonist, nalbuphine (0.6 mg/kg, i.v.). This is probably due to nalbuphine's mu antagonistic action

Systemically administered peptain-1 inhibits retinal ganglion cell death in animal models: implications for neuroprotection in glaucoma.

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Axonal degeneration and death of retinal ganglion cells (RGCs) are the primary causes of vision loss in glaucoma. In this study, we evaluated the efficacy of a peptide (peptain-1) that exhibits robust chaperone and anti-apoptotic activities against RGC loss in two rodent models and in cultured RGCs.

Quercetin Declines Apoptosis, Ameliorates Mitochondrial Function and Improves Retinal Ganglion Cell Survival and Function in In Vivo Model of Glaucoma in Rat and Retinal Ganglion Cell Culture In Vitro.

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Glaucoma is a progressive neuropathy characterized by the loss of retinal ganglion cells (RGCs). Strategies that delay or halt RGC loss have been recognized as potentially beneficial for rescuing vision in glaucoma patients. Quercetin (Qcn) is a natural and important dietary flavonoid compound,

Neuroglobin is an endogenous neuroprotectant for retinal ganglion cells against glaucomatous damage.

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Neuroglobin (NGB), a newly discovered member of the globin superfamily, may regulate neuronal survival under hypoxia or oxidative stress. Although NGB is greatly expressed in retinal neurons, the biological functions of NGB in retinal diseases remain largely unknown. We investigated the role of NGB

Topical Curcumin Nanocarriers are Neuroprotective in Eye Disease.

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Curcumin (1,7-bis-(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5dione) is a polyphenol extracted from turmeric that has long been advocated for the treatment of a variety of conditions including neurodegenerative and inflammatory disorders. Despite this promise, the clinical use of curcumin has been

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