scholarly journals Erythropoietin with Retrobulbar Administration Protects Retinal Ganglion Cells from Acute Elevated Intraocular Pressure in Rats

2008 ◽  
Vol 24 (5) ◽  
pp. 453-460 ◽  
Author(s):  
Yi-sheng Zhong ◽  
Xiao-hong Liu ◽  
Yu Cheng ◽  
Ying-jun Min
2015 ◽  
Vol 117 ◽  
pp. 136
Author(s):  
Jianzhong Ji ◽  
Peter Chang ◽  
Mark E. Pennesi ◽  
Zhuo Yang ◽  
Jian Zhang ◽  
...  

Author(s):  
Shadi Rajabi ◽  
Craig A. Simmons ◽  
C. Ross Ethier

Glaucoma, a chronic optic neuropathy, is the second most common cause of blindness, affecting 67 million people worldwide. The damage in glaucoma occurs at the optic nerve head (ONH), where the axons of the retinal ganglion cells leave the eye posteriorly. Glaucoma is frequently associated with elevated intraocular pressure (IOP), and visual field loss can be prevented by significant lowering of IOP. Hence, the role of pressure in glaucoma is important. Unfortunately, the mechanism by which pressure leads to vision loss in glaucoma is very poorly understood.


Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3158
Author(s):  
Annagrazia Adornetto ◽  
Laura Rombolà ◽  
Luigi Antonio Morrone ◽  
Carlo Nucci ◽  
Maria Tiziana Corasaniti ◽  
...  

Glaucoma, a leading cause of irreversible blindness worldwide, is an optic neuropathy characterized by the progressive death of retinal ganglion cells (RGCs). Elevated intraocular pressure (IOP) is recognized as the main risk factor. Despite effective IOP-lowering therapies, the disease progresses in a significant number of patients. Therefore, alternative IOP-independent strategies aiming at halting or delaying RGC degeneration is the current therapeutic challenge for glaucoma management. Here, we review the literature on the neuroprotective activities, and the underlying mechanisms, of natural compounds and dietary supplements in experimental and clinical glaucoma.


2011 ◽  
Vol 5 (2) ◽  
pp. 195-203 ◽  
Author(s):  
Yi-sheng Zhong ◽  
Min-hong Xiang ◽  
Wen Ye ◽  
Ping Huang ◽  
Yu Cheng ◽  
...  

Abstract Background: Retinal ganglion cells (RGCs) are protected in rats with acute elevated intraocular pressure (IOP) by Erigeron breviscapus (vant.) hand-mazz (EBHM). However, it is unclear whether EBHM has neuroprotective effect on RGCs in animal with chronic elevated IOP. Objective: Investigate the protective effect of EBHM extract on RGCs in rabbits with chronic elevated IOP. Methods: Unilateral chronic elevated IOP was produced in rabbits by repeated injection of 2% methylcellulose into the anterior chamber. Secondary degeneration was measured with and without EBHM extract treatment for 60 days. At 60 days, the cells density of the RGCs layer, the thickness of retinal nerve fiber layer (RNFL), and the optic nerve axons were observed and analyzed using an image analysis system. The ultrastructural changes of RGCs and optic nerve axons were observed using transmission electron microscopy. Results: Compared with their contralateral control eyes with normal IOP, in the retinas of 3-4 mm from the optic disc, the cells density of the RGCs layer in the eyes with chronic elevated IOP was 23.2±6.5 cells (n = 6) and 36.0±8.9 cells (n = 10) per three 400x fields at 60 days in untreated and EBHM-treated group, respectively. The RNFL thickness in eyes with chronic elevated IOP was 3.4±0.4 μm (n = 6) and 5.0±1.0 μm (n = 10) at 60 days in untreated and EBHM-treated group, respectively. The axons number per 15057.8 μm2 in eyes with chronic elevated IOP was 370.4±41.0 (n = 6) and 439.0±50.8 (n = 10) at 60 days in untreated and EBHM-treated group, respectively. The number of the organelles in RGCs plasm appeared decreased and mitochondrion vacuolated in the elevated IOP eyes of EBHM-treated group, while some dispersive mitochondrion and rough surfaced endoplasmic reticulum and ribosome still existed in the RGCs plasm. The myelin sheath plates condensed and degenerated, and the microfilaments and microtubules decreased or disappeared in the elevated IOP eyes, but the axons degeneration in the chronic elevated IOP with EBHM treatment was less than that in the chronic elevated IOP without treatment. Conclusion: EBHM extract provided a neuroprotective effect on retinal ganglion cells in rabbits with chronic elevated IOP.


2020 ◽  
Author(s):  
Nolan R. McGrady ◽  
Dorota L. Stankowska ◽  
Hayden B. Jefferies ◽  
Raghu R. Krishnamoorthy

AbstractPurposeGlaucoma is a neurodegenerative disease associated with elevated intraocular pressure and characterized by optic nerve axonal degeneration, cupping of the optic disc and loss of retinal ganglion cells (RGCs). The endothelin (ET) system of vasoactive peptides (ET-1, ET-2, ET-3) and their G-protein coupled receptors (ETA and ETB receptors) have been shown to be contributors to the pathophysiology of glaucoma. The purpose of this study was to determine if administration of the endothelin receptor antagonist, macitentan, after the onset of IOP elevation, was neuroprotective to retinal ganglion cells in ocular hypertensive rats.MethodsBrown Norway rats were subjected to the Morrison model of ocular hypertension by injection of hypertonic saline through episcleral veins. Macitentan (5 and 10 mg/kg body wt/day) was administered orally following the elevation of IOP and rats with IOP elevation were maintained for 4 weeks. RGC function was determined by pattern electroretinography at 2 and 4 weeks post IOP elevation. Rats were euthanized by approved humane methods and retinal flat-mounts generated were immunostained with RGC-selective markers RBPMS and Brn3a. RGC counts were conducted in a masked manner.ResultsA significant protection of retinal ganglion cells against cell loss was found following oral administration of macitentan (5 and 10 mg/kg body wt/day) in rats with elevated intraocular pressure. In addition, treatment with macitentan was able to preserve RGC function as measured by pattern ERG analysis.ConclusionsMacitentan was able to promote neuroprotection independent of IOP-lowering suggesting that this could complement existing treatments to prevent neurodegeneration during ocular hypertension. The findings presented have implications for the use of macitentan as an oral formulation to promote neuroprotection in glaucoma patients.


2005 ◽  
Vol 45 (2) ◽  
pp. 169-179 ◽  
Author(s):  
Jianzhong Ji ◽  
Peter Chang ◽  
Mark E. Pennesi ◽  
Zhuo Yang ◽  
Jian Zhang ◽  
...  

Author(s):  
Baptiste Coudrillier ◽  
Kristin M. Myers ◽  
Thao D. Nguyen

By 2010, 60 million people will have glaucoma, the second leading cause of blindness worldwide [1]. The disease is characterized by a progressive degeneration of the retinal ganglion cells (RGC), a type of neuron that transmits visual information to the brain. It is well know that elevated intraocular pressure (IOP) is a risk factor in the damage to the RGCs [3–5], but the relationship between the mechanical properties of the ocular connective tissue and how it affects cellular function is not well characterized. The cornea and the sclera are collage-rich structures that comprise the outer load-bearing shell of the eye. Their preferentially aligned collagen lamellae provide mechanical strength to resist ocular expansion. Previous uniaxial tension studies suggest that altered viscoelastic material properties of the eye wall play a role in glaucomatous damage [6].


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