scholarly journals Protective Effects of Oroxylin A on Retinal Ganglion Cells in Experimental Model of Anterior Ischemic Optic Neuropathy

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 902
Author(s):  
Jia-Ying Chien ◽  
Shu-Fang Lin ◽  
Yu-Yau Chou ◽  
Chi-Ying F. Huang ◽  
Shun-Ping Huang
Keyword(s):  
Retinal Ganglion Cells ◽  
Optic Neuropathy ◽  
Ganglion Cells ◽  
Ischemic Injury ◽  
Anterior Ischemic Optic Neuropathy ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Oroxylin A

Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute vision loss in older people, and there is no effective therapy. The effect of the systemic or local application of steroids for NAION patients remains controversial. Oroxylin A (OA) (5,7-dihydroxy-6-methoxyflavone) is a bioactive flavonoid extracted from Scutellariae baicalensis Georgi. with various beneficial effects, including anti-inflammatory and neuroprotective effects. A previous study showed that OA promotes retinal ganglion cell (RGC) survival after optic nerve (ON) crush injury. The purpose of this research was to further explore the potential actions of OA in ischemic injury in an experimental anterior ischemic optic neuropathy (rAION) rat model induced by photothrombosis. Our results show that OA efficiently attenuated ischemic injury in rats by reducing optic disc edema, the apoptotic death of retinal ganglion cells, and the infiltration of inflammatory cells. Moreover, OA significantly ameliorated the pathologic changes of demyelination, modulated microglial polarization, and preserved visual function after rAION induction. OA activated nuclear factor E2 related factor (Nrf2) signaling and its downstream antioxidant enzymes NAD(P)H:quinone oxidoreductase (NQO-1) and heme oxygenase 1 (HO-1) in the retina. We demonstrated that OA activates Nrf2 signaling, protecting retinal ganglion cells from ischemic injury, in the rAION model and could potentially be used as a therapeutic approach in ischemic optic neuropathy.

Efficacy of Vincamine treatment in a rat model of anterior ischemic optic neuropathy

2020 ◽  
pp. 112067212097428
Author(s):  
Lu Li ◽  
Yu Su ◽  
Juejun Liu ◽  
Changzheng Chen
Keyword(s):  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Optic Neuropathy ◽  
Rat Model ◽  
Ganglion Cells ◽  
Nutrition Therapy ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Ischemic Tissue

Non-arteritic anterior ischemic optic neuropathy (NAION) is characterized by the progressive and irreversible death of retinal ganglion cells (RGCs) which is caused by the insufficient blood supply to the optic nerve (ON) head. At present, hormone therapy is used to reduce optic edema, followed by nerve nutrition therapy to protect the ON. However, no surgical or medical therapy has proven to be beneficial consistently in treating NAION. Vincamine is an alkaloid extracted from the Apocynaceae Vinca plant. Vincamine and its derivatives acting as cerebral vasodilators can easily cross the blood-brain barrier, improve the metabolism of ischemic tissue and protect the neuron. In this study, we aimed to investigate the potential neuroprotection of Vincamine in the photodynamic induced rat model of NAION (rAION), to evaluate its effects and possible mechanisms. We found that Vincamine can rescue RGC death and reduce the number of apoptotic cells. The protection of Vincamine might play through the PI3K/Akt/eNOS signaling pathway. Therefore, Vincamine can be an effective therapy method for NAION.

scholarly journals Dimethyl Fumarate Promotes the Survival of Retinal Ganglion Cells after Optic Nerve Injury, Possibly through the Nrf2/HO-1 Pathway

2020 ◽  
Vol 22 (1) ◽  
pp. 297
Author(s):  
Sotaro Mori ◽  
Takuji Kurimoto ◽  
Hidetaka Maeda ◽  
Makoto Nakamura
Keyword(s):  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Rna Binding ◽  
Ganglion Cells ◽  
Dimethyl Fumarate ◽  
Daily Administration ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Retinal Ganglion ◽  
Nerve Crush

This study aimed to verify whether dimethyl fumarate (DMF) promotes the survival of retinal ganglion cells (RGCs) after optic nerve crush (ONC) accompanied by activation of the NF-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. We examined changes in the densities of tubulin β3 (TUBB3)-positive RGCs and the amplitudes of the positive scotopic threshold response (pSTR), reflecting the functional activity of RGCs, recorded on an electroretinogram, with daily administration of DMF, on day 7 after ONC. Furthermore, immunohistochemical and immunoblotting analyses were performed to study the activation of the Nrf2/HO-1 pathway using retinas treated with daily administration of DMF. Daily administration of DMF increasedthe density of TUBB3-positive RGCs in a dose-dependent fashion and significantly increased the amplitude of the pSTR. Immunohistochemical analysis showed that DMF administration increased the immunoreactivity for Nrf2 and HO-1, a potent antioxidant enzyme, in RGCs immunolabeled with RNA-binding protein with multiple splicing (RBPMS). Immunoblotting analysis revealed an increase in the nuclear expression of Nrf2 and marked upregulation of HO-1 after DMF administration. These results suggest that DMF has survival-promoting effects in RGC after ONC, possibly via the Nrf2/HO-1 pathway.

scholarly journals Protective effects of quercetin in a rodent model of anterior ischemic optic neuropathy (rAION)

2019 ◽  
Author(s):  
Ya-nan Lyu ◽  
Jing-yu Min ◽  
Yuanyuan Gong ◽  
qing Gu ◽  
fang Wei
Keyword(s):  
Intravitreal Injection ◽  
Optic Neuropathy ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Rodent Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Protective Effects ◽  
High Power Field ◽  
Optic Nerves

Abstract Background: Anterior ischemic optic neuropathy (AION) is the leading cause of sudden optic nerve-related (ON-related) vision loss in elderly people. However, no considerable treatments are available for the neuroprotection of NAION. The purpose of this study was to detect the effects of intravitreal injection of quercetin (Qcn) in a rodent model of anterior ischemic optic neuropathy (rAION). Methods: The rAION model was established using verteporfin and laser in a photodynamic procedure on the optic discs (ON) of rats. The rats received intravitreal injection of Qcn 2 days before the injury and once/week for 4 weeks after the infarct on optic neuropathy. Flash-visual evoked potential (VEP) were recorded to assess the visual function. TUNEL and retrograde Fluorogold labeling assessed the apoptosis and density of retinal ganglion cells (RGCs). ED-1 and Iba-1 staining of the optic nerves displayed the inflammatory response. Results: At 14 days post-infarct, Qcn treatment significantly reduced the number of apoptotic RGCs, as well as, ED1/Iba-1-positive cells/high power field(HPF) in the ON (p<0.01) as compared to the rAION group. At week 4 after rAION, 28.4% VEP amplitudes were estimated in the treated eyes of the fellow eyes in the rAION group and 64.7% in the rAION+Qcn group (p<0.01). In addition, Qcn saved the RGCs in the central retinas as compared to those of the rAION group (1967.5±162.1 and 2868±325.3 mm2, respectively (p<0.01), and the corresponding densities were 1654.8±104.8 and 2208±272.9 mm2 in the mid-peripheral retinas, respectively (p<0.01). Conclusion: The intravitreal injection of Qcn could protect the RGCs from injury in the rAION animal model, as demonstrated anatomically by RGC density and functionally by F-VEP. Moreover, Qcn might exert an anti-apoptosis role in the survival of RGCs and anti-inflammatory in the optic nerves.

scholarly journals Oxidative Stress in Optic Neuropathies

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1538
Author(s):  
Berta Sanz-Morello ◽  
Hamid Ahmadi ◽  
Rupali Vohra ◽  
Sarkis Saruhanian ◽  
Kristine Karla Freude ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Optic Neuropathy ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Redox System ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Oxidative Stress Biomarkers ◽  
Optic Disc Drusen ◽  
Advanced Stages

Increasing evidence indicates that changes in the redox system may contribute to the pathogenesis of multiple optic neuropathies. Optic neuropathies are characterized by the neurodegeneration of the inner-most retinal neurons, the retinal ganglion cells (RGCs), and their axons, which form the optic nerve. Often, optic neuropathies are asymptomatic until advanced stages, when visual impairment or blindness is unavoidable despite existing treatments. In this review, we describe systemic and, whenever possible, ocular redox dysregulations observed in patients with glaucoma, ischemic optic neuropathy, optic neuritis, hereditary optic neuropathies (i.e., Leber’s hereditary optic neuropathy and autosomal dominant optic atrophy), nutritional and toxic optic neuropathies, and optic disc drusen. We discuss aspects related to anti/oxidative stress biomarkers that need further investigation and features related to study design that should be optimized to generate more valuable and comparable results. Understanding the role of oxidative stress in optic neuropathies can serve to develop therapeutic strategies directed at the redox system to arrest the neurodegenerative processes in the retina and RGCs and ultimately prevent vision loss.

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