Displaying publications 1 - 20 of 29 in total

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  1. Norhani Mohidin, Shaznida Ghulam, Rokiah Omar
    MyJurnal
    Elektroretinogram paten (pERG) adalah pengrekodan respons retina terhadap stimulus paten yang dipancarkan bersilih ganti. Ia memberi maklumat mengenai integriti sel dalaman retina khasnya sel ganglion. Pengrekodan pERG dalam sesebuah makmal boleh dipengaruhi oleh beberapa faktor, maka piawai makmal perlu ada untuk memastikan bacaan pERG yang diperolehi boleh diulang dan dihasilkan semula. Objektif kajian ini ialah untuk menentusahkan faktor yang mungkin mempengaruhi pengukuran pERG untuk paiwaian Makmal Elektrofisiologi Jabatan Optometri, Fakulti Sains Kesihatan (FSK), Universiti Kebangsaan Malaysia (UKM). Kajian ini melibatkan 45 orang subjek yang berumur di antara 20 hingga 25 tahun yang dibahagikan kepada 3 kumpulan. Faktor yang dikaji adalah 1) kesan penggunaan anestetik Alcaine 0.5%, 2) variasi pengukuran pada waktu pagi dan petang dan 3) saiz dan bentuk target fiksasi yang berbeza terhadap bacaan pERG (amplitud dan tempoh pendam). Ujian-t berpasangan mendapati tiada perbezaan yang signifikan antara pengukuran sebelum dan selepas penggunaan Alcaine 0.5% bagi amplitud (p = 0.116) dan tempoh pendam
    (p = 0.557). Pengukuran pada waktu pagi dan petang juga menunjukkan tiada perbezaan signifikan bagi amplitud (p = 0.864) dan tempoh pendam (p = 0.174). Untuk bentuk dan saiz target yang berbeza, didapati tiada perbezaan yang signifikan untuk parameter amplitud (p = 0.125) dan tempoh pendam (p = 0.404). Kesimpulannya, penggunaan Alcaine 0.5%, pengukuran pada waktu pagi dan petang dan target fiksasi yang berbeza tidak mempengaruhi bacaan pERG di Makmal Elektrofisiologi, FSK, UKM. Hasil kajian boleh diguna pakai untuk perbandingan dalam penyelidikan ataupun tujuan pendiagnosan penyakit retina di masa hadapan.


    Matched MeSH terms: Retinal Ganglion Cells
  2. Agarwal R, Agarwal P, Iezhitsa I
    Expert Opin Drug Discov, 2023;18(11):1287-1300.
    PMID: 37608634 DOI: 10.1080/17460441.2023.2246892
    INTRODUCTION: Animal models are widely used in glaucoma-related research. Since the elevated intraocular pressure (IOP) is a major risk factor underlying the disease pathogenesis, animal models with high IOP are commonly used. However, models are also used to represent the clinical context of glaucomatous changes developing despite a normal IOP.

    AREAS COVERED: Herein, the authors discuss the various factors that contribute to the quality of studies using animal models based on the evaluation of studies published in 2022. The factors affecting the quality of studies using animal models, such as the animal species, age, and sex, are discussed, along with various methods and outcomes of studies involving different animal models of glaucoma.

    EXPERT OPINION: Translating animal research data to clinical applications remains challenging. Our observations in this review clearly indicate that many studies lack scientific robustness not only in their experiment conduct but also in data analysis, interpretation, and presentation. In this context, ensuring the internal validity of animal studies is the first step in quality assurance. External validity, however, is more challenging, and steps should be taken to satisfy external validity at least to some extent.

    Matched MeSH terms: Retinal Ganglion Cells/pathology
  3. Agarwal R, Agarwal P
    Indian J Ophthalmol, 2012 Jul;60(4):255-61.
    PMID: 22824592 DOI: 10.4103/0301-4738.98700
    Glaucoma, a neurodegenerative disease, is currently being treated by modulation of one of its primary risk factors, the elevated intraocular pressure. Newer therapies that can provide direct neuroprotection to retinal ganglion cells are being extensively investigated. Tumor necrosis factor-α, a cytokine, has been recognized to play an important role in pro and antiapoptotic cellular events. In this paper we review the relevant literature to understand (1) The association of increased expression of tumor necrosis factor-α with glaucomatous neurodegeneraion, (2) Modulation of tumor necrosis factor-α expression by exposure to various risk factors of glaucoma, (3) Downstream cellular signaling mechanisms following interaction of tumor necrosis factor-α with its receptors and (4) Role of tumor necrosis factor-α as a possible target for therapeutic intervention in glaucoma. Literature was reviewed using PubMed search engine with relevant key words and a total of 82 English language papers published from 1990 to 2010 are included in this review.
    Matched MeSH terms: Retinal Ganglion Cells/metabolism; Retinal Ganglion Cells/pathology*
  4. Ooi YL, Khang TF, Naidu M, Fong KC
    Eye (Lond), 2013 Mar;27(3):425-31.
    PMID: 23196646 DOI: 10.1038/eye.2012.260
    To compare the potential retinal toxicity of two commercially Brilliant blue G dyes (Brilliant Peel and Ocublue Plus) and Indocyanine green (ICG) at usual clinical concentration.
    Matched MeSH terms: Retinal Ganglion Cells/drug effects; Retinal Ganglion Cells/pathology
  5. Fazel MF, Abu IF, Mohamad MHN, Agarwal R, Iezhitsa I, Bakar NS, et al.
    PLoS One, 2020;15(7):e0236450.
    PMID: 32706792 DOI: 10.1371/journal.pone.0236450
    Retinal ganglion cell (RGC) loss and optic neuropathy, both hallmarks of glaucoma, have been shown to involve N-methyl-D-aspartate receptor (NMDAR)-mediated excitotoxicity. This study investigated the neuroprotective effects of Philanthotoxin (PhTX)-343 in NMDA-induced retinal injury to alleviate ensuing visual impairments. Sprague-Dawley rats were divided into three; Group I was intravitreally injected with phosphate buffer saline as the control, Group II was injected with NMDA (160 nM) to induce retinal excitotoxic injury, while Group III was injected with PhTX-343 (160 nM) 24 h prior to excitotoxicity induction with NMDA. Rats were subjected to visual behaviour tests seven days post-treatment and subsequently euthanized. Rat retinas and optic nerves were subjected to H&E and toluidine blue staining, respectively. Histological assessments showed that NMDA exposure resulted in significant loss of retinal cell nuclei and thinning of ganglion cell layer (GCL). PhTX-343 pre-treatment prevented NMDA-induced changes where the RGC layer morphology is similar to the control. The numbers of nuclei in the NMDA group were markedly lower compared to the control (p<0.05). PhTX-343 group had significantly higher numbers of nuclei within 100 μm length and 100 μm2 area of GCL (2.9- and 1.7-fold, respectively) compared to NMDA group (p<0.05). PhTX-343 group also displayed lesser optic nerve fibres degeneration compared to NMDA group which showed vacuolation in all sections. In the visual behaviour test, the NMDA group recorded higher total distance travelled, and lower total immobile time and episodes compared to the control and PhTX-343 groups (p<0.05). Object recognition tests showed that the rats in PhTX-343 group could recognize objects better, whereas the same objects were identified as novel by NMDA rats despite multiple exposures (p<0.05). Visual performances in the PhTX-343 group were all comparable with the control (p>0.05). These findings suggested that PhTX-343 inhibit retinal cell loss, optic nerve damage, and visual impairments in NMDA-induced rats.
    Matched MeSH terms: Retinal Ganglion Cells/drug effects*; Retinal Ganglion Cells/pathology
  6. Arfuzir NN, Lambuk L, Jafri AJ, Agarwal R, Iezhitsa I, Sidek S, et al.
    Neuroscience, 2016 06 14;325:153-64.
    PMID: 27012609 DOI: 10.1016/j.neuroscience.2016.03.041
    Vascular dysregulation has long been recognized as an important pathophysiological factor underlying the development of glaucomatous neuropathy. Endothelin-1 (ET1) has been shown to be a key player due to its potent vasoconstrictive properties that result in retinal ischemia and oxidative stress leading to retinal ganglion cell (RGC) apoptosis and optic nerve (ON) damage. In this study we investigated the protective effects of magnesium acetyltaurate (MgAT) against retinal cell apoptosis and ON damage. MgAT was administered intravitreally prior to, along with or after administration of ET1. Seven days post-injection, animals were euthanized and retinae were subjected to morphometric analysis, TUNEL and caspase-3 staining. ON sections were stained with toluidine blue and were graded for neurodegenerative effects. Oxidative stress was also estimated in isolated retinae. Pre-treatment with MgAT significantly lowered ET1-induced retinal cell apoptosis as measured by retinal morphometry and TUNEL staining. This group of animals also showed significantly lesser caspase-3 activation and significantly reduced retinal oxidative stress compared to the animals that received intravitreal injection of only ET1. Additionally, the axonal degeneration in ON was markedly reduced in MgAT pretreated animals. The animals that received MgAT co- or post-treatment with ET1 also showed improvement in all parameters; however, the effects were not as significant as observed in MgAT pretreated animals. The current study showed that the intravitreal pre-treatment with MgAT reduces caspase-3 activation and prevents retinal cell apoptosis and axon loss in ON induced by ET1. This protective effect of ET1 was associated with reduced retinal oxidative stress.
    Matched MeSH terms: Retinal Ganglion Cells/drug effects; Retinal Ganglion Cells/metabolism; Retinal Ganglion Cells/pathology*
  7. Agarwal R
    Medical Health Reviews, 2009;2009(1):75-93.
    MyJurnal
    Glaucoma, recognized as optic neuropathy is the second largest cause of blindness worldwide. The disease is characterized by progressive loss of retinal ganglion cells and visual field defects. The pathophysiological factors involved in the onset and progression of glaucoma are not fully understood. However, it is now well accepted that elevated intraocular pressure is not the only causative factor. The pathophysiology of glaucoma involves multiple factors that interact in a highly complex manner to favor development of glaucomatous optic neuropathy. As the knowledge of molecular mechanisms involved is expanding, more and more therapeutic targets are being recognized for the development of safe and effective pharmacotherapy of glaucoma. Although at present the intraocular pressure lowering drugs are still the first line of treatment, the prospect of introducing neuroprotective therapies that can directly protect and perhaps stimulate regeneration of dying and dead retinal ganglion cells, shows considerable promise. This review presents recent developments in the pathophysiology and pharmacotherapy of glaucoma.
    Matched MeSH terms: Retinal Ganglion Cells
  8. Ahmad SS
    Saudi J Ophthalmol, 2017 Jan-Mar;31(1):38-41.
    PMID: 28337061 DOI: 10.1016/j.sjopt.2016.08.001
    Glaucoma is a multi-factorial neurodegenerative disorder. The common denominator in all types of glaucomas is retinal ganglion cell death through apoptosis. However, this cellular demise in glaucoma is detected late by structural or functional analyses. There can be a 10-year delay prior to the appearance of visual field defects and pre-perimetric glaucoma is an issue still being addressed. However, a new cutting-edge technology called detection of apoptosing retinal cells (DARC) is being developed. This technique is capable of non-invasive, real-time visualization of apoptotic changes at the cellular level. It can detect glaucomatous cell damage at a very early stage, at the moment apoptosis starts, and thus management can be initiated even prior to development of visual field changes. In future, this technique will also be able to provide conclusive evidence of the effectiveness of treatment protocol and the need for any modifications which may be required. This article aims to provide a concise review of DARC technology.
    Matched MeSH terms: Retinal Ganglion Cells
  9. Ngoo QZ, A NF, A B, Wh WH
    Korean J Ophthalmol, 2021 06;35(3):223-230.
    PMID: 34120421 DOI: 10.3341/kjo.2020.0019
    PURPOSE: To study the retinal nerve fiber layer (RNFL) thickness and optic nerve head (ONH) parameters in obstructive sleep apnoea (OSA) patients and their relationship with severity of the disease.

    METHODS: A cross-sectional, hospital-based study. Fifty-four OSA subjects and 54 controls were recruited. Candidate that fulfil the criteria with normal ocular examinations then proceed with spectrum domain Cirrus optical coherence tomography examinations. ONH parameters and RNFL thickness were evaluated. Apnoea-hypopnoea index (AHI) of the OSA group were obtained from the medical record.

    RESULTS: In OSA, mean of average RNFL thickness was 93.87 µm, standard deviation (SD) = 9.17, p = 0.008 (p < 0.05) while superior RNFL thickness was 113.59 µm, SD = 16.29, p ≤ 0.001 (p < 0.05). RNFL thickness fairly correlate with severity of the disease (AHI), superior RNFL with R = 0.293, R2 = 0.087, p = 0.030 (p < 0.05), and nasal RNFL R = 0.292, R2 = 0.085, p = 0.032. No significant difference and correlation observed on ONH parameters. In control group, mean of average RNFL thickness was 98.96 µm, SD = 10.50, p = 0.008 (p < 0.05) while superior RNFL thickness was 125.76 µm, SD = 14.93, p ≤ 0.001 (p < 0.05).

    CONCLUSIONS: The mean of the average and superior RNFL thickness were significantly lower in the OSA group compare to control. Regression analysis showed RNFL thickness having significantly linear relationship with the AHI, specifically involving the superior and nasal quadrant.

    Matched MeSH terms: Retinal Ganglion Cells
  10. Ling KP, Mangalesh S, Tran-Viet D, Gunther R, Toth CA, Vajzovic L
    Retina, 2020 Oct;40(10):1996-2003.
    PMID: 31764609 DOI: 10.1097/IAE.0000000000002688
    BACKGROUND/PURPOSE: Using handheld spectral domain optical coherence tomography (SDOCT) imaging to investigate in vivo microanatomic retinal changes and their progression over time in young children with juvenile X-linked retinoschisis (XLRS).

    METHODS: This retrospective analysis was of handheld SD OCT images obtained under a prospective research protocol in children who had established XLRS diagnosis based on genetic testing or clinical history. Three OCT graders performed standardized qualitative and quantitative assessment of retinal volume scans, which were divided into foveal, parafoveal, and extrafoveal regions. Visual acuity data were obtained when possible.

    RESULTS: Spectral domain OCT images were available of both eyes in 8 pediatric patients with ages 7 months to 10 years. The schisis cavities involved inner nuclear layer in over 90% (15/16) of eyes in all 3 regions. Retinal nerve fiber and ganglion cell layer involvement was present only in the extrafoveal region in 63% (10/16) eyes and outer nuclear and plexiform layer in few others. In 7 children followed over 2 months to 15 months, the location of schisis remained consistent. Central foveal thickness decreased from the baseline to final available visit in 4/6 eyes. Ellipsoid zone disruption seemed to accompany lower visual acuity in 1/4 eyes.

    CONCLUSION: Early in life, the SD OCT findings in XLRS demonstrate differences in schisis location in fovea-parafoveal versus extrafoveal region, possible association between poor visual acuity and degree of ellipsoid zone disruption and decrease in central foveal thickness over time in this group. Furthermore, they illustrates that the pattern of XLRS in adults is already present in very young children, and unlike in older children and adults, those presenting with earlier disease may have a more aggressive course. Further studies in this early age group may provide more insights into treatment and prevention of progressive visual impairment in children with XLRS.

    Matched MeSH terms: Retinal Ganglion Cells/pathology
  11. Nor Arfuzir NN, Agarwal R, Iezhitsa I, Agarwal P, Ismail NM
    Exp Eye Res, 2020 05;194:107996.
    PMID: 32156652 DOI: 10.1016/j.exer.2020.107996
    Endothelin-1 (ET-1), a potent vasoconstrictor, plays a significant role in the pathophysiology of ocular conditions like glaucoma. Glaucoma is characterized by apoptotic loss of retinal ganglion cells (RGCs) and loss of visual fields and is a leading cause of irreversible blindness. In glaucomatous eyes, retinal ischemia causes release of pro-inflammatory mediators such as interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α and promotes activation of transcription factors such as nuclear factor kappa B (NFKB) and c-Jun. Magnesium acetyltaurate (MgAT) has previously been shown to protect against ET-1 induced retinal and optic nerve damage. Current study investigated the mechanisms underlying these effects of MgAT, which so far remain unknown. Sprague dawley rats were intravitreally injected with ET-1 with or without pretreatment with MgAT. Seven days post-injection, retinal expression of IL-1β, IL-6, TNF-α, NFKB and c-Jun protein and genes was determined using multiplex assay, Western blot and PCR. Animals were subjected to retrograde labeling of RGCs to determine the extent of RGC survival. RGC survival was also examined using Brn3A staining. Furthermore, visual functions of rats were determined using Morris water maze. It was observed that pre-treatment with MgAT protects against ET-1 induced increase in the retinal expression of IL-1β, IL-6 and TNF-α proteins and genes. It also protected against ET-1 induced activation of NFKB and c-Jun. These effects of MgAT were associated with greater RGC survival and preservation of visual functions in rats. In conclusion, MgAT prevents ET-1 induced RGC loss and loss of visual functions by suppressing neuroinflammatory reaction in rat retinas.
    Matched MeSH terms: Retinal Ganglion Cells/drug effects*; Retinal Ganglion Cells/pathology
  12. Nor Arfuzir NN, Agarwal R, Iezhitsa I, Agarwal P, Sidek S, Spasov A, et al.
    Curr Eye Res, 2018 08;43(8):1032-1040.
    PMID: 29676937 DOI: 10.1080/02713683.2018.1467933
    PURPOSE: Retinal ganglion cell apoptosis in glaucoma is associated with elevated levels of endothelin-1 (ET1), a potent vasoconstrictor. ET1-induced retinal ischemia leads to altered expression of nitric oxide synthase (NOS) isoforms leading to increased formation of nitric oxide (NO) and retinal nitrosative stress. Since magnesium (Mg) is known to improve endothelial functions and reduce oxidative stress and taurine (TAU) possesses potent antioxidant properties, we investigated the protective effects of magnesium acetyltaurate (MgAT) against ET1-induced nitrosative stress and retinal damage in rats. We also compared the effects of MgAT with that of TAU alone.

    METHODS: Sprague Dawley rats were intravitreally injected with ET1. MgAT and TAU were administered as pre-, co-, or posttreatment. Subsequently, the expression of NOS isoforms was detected in retina by immunohistochemistry, retinal nitrotyrosine level was estimated using ELISA, and retinal cell apoptosis was detected by TUNEL staining.

    RESULTS: Intravitreal ET1 caused a significant increase in the expressions of nNOS and iNOS while eNOS expression was significantly reduced compared to vehicle treated group. Administration of both MgAT and TAU restored the altered levels of NOS isoform expression, reduced retinal nitrosative stress and retinal cell apoptosis. The effect of MgAT, however, was greater than that of TAU alone.

    CONCLUSIONS: MgAT and TAU prevent ET1-induced retinal cell apoptosis by reducing retinal nitrosative stress in Sprague Dawley rats. Addition of TAU to Mg seems to enhance the efficacy of TAU compared to when given alone. Moreover, the pretreatment with MgAT/TAU showed higher efficacy compared to co- or posttreatment.

    Matched MeSH terms: Retinal Ganglion Cells/drug effects; Retinal Ganglion Cells/metabolism*
  13. Mohd Lazaldin MA, Iezhitsa I, Agarwal R, Bakar NS, Agarwal P, Mohd Ismail N
    Eur J Neurosci, 2020 06;51(12):2394-2411.
    PMID: 31883161 DOI: 10.1111/ejn.14662
    Brain-derived neurotrophic factor (BDNF) could be considered a potential neuroprotective therapy in amyloid beta (Aβ)-associated retinal and optic nerve degeneration. Hence, in this study we investigated the neuroprotective effect of BDNF against Aβ1-40-induced retinal and optic nerve injury. In this study, exposure to Aβ1-40 was associated with retinal and optic nerve injury. TUNEL staining showed significant reduction in the apoptotic cell count in the BDNF-treated group compared with Aβ1-40 group. H&E-stained retinal sections also showed a striking reduction in neuronal cells in the ganglion cell layer (GCL) of retinas fourteen days after Aβ1-40 exposure. By contrast, number of retinal cells was preserved in the retinas of BDNF-treated animals. After Aβ1-40 exposure, visible axonal swelling was observed in optic nerve sections. However, the BDNF-treated group showed fewer changes in optic nerve; axonal swelling was less frequent and less marked. In the present study, exposure to Aβ was associated with oxidative stress, whereas levels of retinal glutathione (GSH), superoxide dismutase (SOD) and catalase were significantly increased in BDNF-treated than in Aβ1-40-treated rats. Both visual object recognition tests using an open-field arena and a Morris water maze showed that BDNF improved rats' ability to recognise visual cues (objects with different shapes) after Aβ1-40 exposure, thus demonstrating that the visual performance of rats was relatively preserved following BDNF treatment. In conclusion, intravitreal treatment with BDNF prevents Aβ1-40-induced retinal cell apoptosis and axon loss in the optic nerve of rats by reducing retinal oxidative stress and restoring retinal BDNF levels.
    Matched MeSH terms: Retinal Ganglion Cells
  14. Mohd-Ilham I, Tai ELM, Suhaimi H, Shatriah I
    Korean J Ophthalmol, 2021 08;35(4):287-294.
    PMID: 34162187 DOI: 10.3341/kjo.2020.0106
    PURPOSE: There are limited data from Asian countries regarding retinal thickness in children with type 1 diabetes mellitus (T1DM). This study aimed to compare the macular and retinal nerve fiber layer (RNFL) parameters between diabetic children without retinopathy and non-diabetic healthy children. We also evaluated the factors associated with RNFL thickness in children with T1DM.

    METHODS: A comparative cross-sectional study was conducted among children with T1DM and healthy children aged 7 to 17 years old in Hospital Universiti Sains Malaysia from 2017 to 2019. Children with retinal disease or glaucoma were excluded. Macular and RNFL thicknesses were measured using spectral-domain optical coherence tomography. Demographic information, duration of diabetes, blood pressure, body mass index, visual acuity, and retinal examination findings were documented. Glycosylated hemoglobin levels, renal function, and blood lipid levels were also collected.

    RESULTS: Forty-one children with T1DM and 80 age- and sex-matched children were enrolled. Both sexes were affected. Mean duration of diabetes mellitus was 3.66 years. The mean glycated hemoglobin levels in the T1DM group was 9.99%. The mean macular and RNFL thicknesses in children with T1DM were 277.56 (15.82) µm and 98.85 (12.05) µm, respectively. Children with T1DM had a significantly thinner average macula, superior outer macula, nasal outer macula, mean RNFL, and inferior RNFL thickness compared to controls (p < 0.05). There was a significant association between nephropathy and the mean RNFL thickness.

    CONCLUSIONS: Children with T1DM had significantly decreased mean macular and RNFL thicknesses. Nephropathy is associated with an increased RNFL thickness.

    Matched MeSH terms: Retinal Ganglion Cells
  15. Lambuk L, Jafri AJ, Arfuzir NN, Iezhitsa I, Agarwal R, Rozali KN, et al.
    Neurotox Res, 2017 01;31(1):31-45.
    PMID: 27568334 DOI: 10.1007/s12640-016-9658-9
    Glutamate excitotoxicity plays a major role in the loss of retinal ganglion cells (RGCs) in glaucoma. The toxic effects of glutamate on RGCs are mediated by the overstimulation of N-methyl-D-aspartate (NMDA) receptors. Accordingly, NMDA receptor antagonists have been suggested to inhibit excitotoxicity in RGCs and delay the progression and visual loss in glaucoma patients. The purpose of the present study was to examine the potential neuroprotective effect of Mg acetyltaurate (MgAT) on RGC death induced by NMDA. MgAT was proposed mainly due to the combination of magnesium (Mg) and taurine which may provide neuroprotection by dual mechanisms of action, i.e., inhibition of NMDA receptors and antioxidant effects. Rats were divided into 5 groups and were given intravitreal injections. Group 1 (PBS group) was injected with vehicle; group 2 (NMDA group) was injected with NMDA while groups 3 (pre-), 4 (co-), and 5 (post-) treatments were injected with MgAT, 24 h before, in combination or 24 h after NMDA injection respectively. NMDA and MgAT were injected in PBS at doses 160 and 320 nmol, respectively. Seven days after intravitreal injection, the histological changes in the retina were evaluated using hematoxylin & eosin (H&E) staining. Optic nerves were dissected and stained in Toluidine blue for grading on morphological neurodegenerative changes. The extent of apoptosis in retinal tissue was assessed by TUNEL assay and caspase-3 immunohistochemistry staining. The estimation of neurotrophic factor, oxidative stress, pro/anti-apoptotic factors and caspase-3 activity in retina was done using enzyme-linked immunosorbent assay (ELISA) technique. The retinal morphometry showed reduced thickness of ganglion cell layer (GCL) and reduction in the number of retinal cells in GCL in NMDA group compared to the MgAT-treated groups. TUNEL and caspase-3 staining showed increased number of apoptotic cells in inner retina. The results were further corroborated by the estimation of neurotrophic factor, oxidative stress, pro/anti-apoptotic factors, and caspase-3 activity in retina. In conclusion, current study revealed that intravitreal MgAT prevents retinal and optic nerve damage induced by NMDA. Overall, our data demonstrated that the pretreatment with MgAT was more effective than co- and posttreatment. This protective effect of MgAT against NMDA-induced retinal cell apoptosis could be attributed to the reduction of retinal oxidative stress and activation of BDNF-related neuroprotective mechanisms.
    Matched MeSH terms: Retinal Ganglion Cells/drug effects*; Retinal Ganglion Cells/metabolism; Retinal Ganglion Cells/pathology
  16. Jafri AJA, Agarwal R, Iezhitsa I, Agarwal P, Spasov A, Ozerov A, et al.
    Mol Vis, 2018;24:495-508.
    PMID: 30090013
    Purpose: Retinal nitrosative stress associated with altered expression of nitric oxide synthases (NOS) plays an important role in excitotoxic retinal ganglion cell loss in glaucoma. The present study evaluated the effects of magnesium acetyltaurate (MgAT) on changes induced by N-methyl-D-aspartate (NMDA) in the retinal expression of three NOS isoforms, retinal 3-nitrotyrosine (3-NT) levels, and the extent of retinal cell apoptosis in rats. Effects of MgAT with taurine (TAU) alone were compared to understand the benefits of a combined salt of Mg and TAU.

    Methods: Excitotoxic retinal injury was induced with intravitreal injection of NMDA in Sprague-Dawley rats. All treatments were given as pre-, co-, and post-treatment with NMDA. Seven days post-injection, the retinas were processed for measurement of the expression of NOS isoforms using immunostaining and enzyme-linked immunosorbent assay (ELISA), retinal 3-NT content using ELISA, retinal histopathological changes using hematoxylin and eosin (H&E) staining, and retinal cell apoptosis using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining.

    Results: As observed on immunohistochemistry, the treatment with NMDA caused a 4.53-fold increase in retinal nNOS expression compared to the PBS-treated rats (p<0.001). Among the MgAT-treated groups, only the pretreatment group showed significantly lower nNOS expression than the NMDA-treated group with a 2.00-fold reduction (p<0.001). Among the TAU-treated groups, the pre- and cotreatment groups showed 1.84- and 1.71-fold reduction in nNOS expression compared to the NMDA-treated group (p<0.001), respectively, but remained higher compared to the PBS-treated group (p<0.01). Similarly, iNOS expression in the NMDA-treated group was significantly greater than that for the PBS-treated group (2.68-fold; p<0.001). All MgAT treatment groups showed significantly lower iNOS expression than the NMDA-treated groups (3.58-, 1.51-, and 1.65-folds, respectively). However, in the MgAT co- and post-treatment groups, iNOS expression was significantly greater than in the PBS-treated group (1.77- and 1.62-folds, respectively). Pretreatment with MgAT caused 1.77-fold lower iNOS expression compared to pretreatment with TAU (p<0.05). In contrast, eNOS expression was 1.63-fold higher in the PBS-treated group than in the NMDA-treated group (p<0.001). Among all treatment groups, only pretreatment with MgAT caused restoration of retinal eNOS expression with a 1.39-fold difference from the NMDA-treated group (p<0.05). eNOS expression in the MgAT pretreatment group was also 1.34-fold higher than in the TAU pretreatment group (p<0.05). The retinal NOS expression as measured with ELISA was in accordance with that estimated with immunohistochemistry. Accordingly, among the MgAT treatment groups, only the pretreated group showed 1.47-fold lower retinal 3-NT than the NMDA-treated group, and the difference was significant (p<0.001). The H&E-stained retinal sections in all treatment groups showed statistically significantly greater numbers of retinal cell nuclei than the NMDA-treated group in the inner retina. However, the ganglion cell layer thickness in the TAU pretreatment group remained 1.23-fold lower than that in the MgAT pretreatment group (p<0.05). In line with this observation, the number of apoptotic cells as observed after TUNEL staining was 1.69-fold higher after pretreatment with TAU compared to pretreatment with MgAT (p<0.01).

    Conclusions: MgAT and TAU, particularly with pretreatment, reduce retinal cell apoptosis by reducing retinal nitrosative stress. Pretreatment with MgAT caused greater improvement in NMDA-induced changes in iNOS and eNOS expression and retinal 3-NT levels than pretreatment with TAU. The greater reduction in retinal nitrosative stress after pretreatment with MgAT was associated with lower retinal cell apoptosis and greater preservation of the ganglion cell layer thickness compared to pretreatment with TAU.

    Matched MeSH terms: Retinal Ganglion Cells/drug effects*; Retinal Ganglion Cells/metabolism; Retinal Ganglion Cells/pathology
  17. Lee WW, Tajunisah I, Sharmilla K, Peyman M, Subrayan V
    Invest Ophthalmol Vis Sci, 2013 Nov;54(12):7785-92.
    PMID: 24135757 DOI: 10.1167/iovs.13-12534
    We determined structural retinal nerve fiber layer (RNFL) changes in schizophrenia patients and established if the structural changes were related to the duration of the illness using spectral-domain optical coherence tomography (SD-OCT).
    Matched MeSH terms: Retinal Ganglion Cells/pathology*
  18. Mohammad Salih PA
    J Glaucoma, 2012 Jan;21(1):41-4.
    PMID: 21173707 DOI: 10.1097/IJG.0b013e3181fc8053
    To investigate the influence of myopia on peripapillary retinal nerve fiber layer (RNFL) thickness using Cirrus optical coherence tomography (OCT) in normal eyes.
    Matched MeSH terms: Retinal Ganglion Cells/pathology*
  19. Khalilpour S, Latifi S, Behnammanesh G, Majid AM, Majid AS, Tamayol A
    J Neurol Sci, 2017 Apr 15;375:430-441.
    PMID: 28320183 DOI: 10.1016/j.jns.2016.12.044
    Optic neuropathy is a neurodegenerative disease which involves optic nerve injury. It is caused by acute or intermittent insults leading to visual dysfunction. There are number of factors, responsible for optic neuropathy, and the optic nerve axon is affected in all type which causes the loss of retinal ganglion cells. In this review we will highlight various mechanisms involved in the cell loss cascades during axonal degeneration as well as ischemic optic neuropathy. These mechanisms include oxidative stress, excitotoxicity, angiogenesis, neuroinflammation and apoptosis following retinal ischemia. We will also discuss the effect of neuroprotective agents in attenuation of the negative effect of factors involve in the disease occurrence and progression.
    Matched MeSH terms: Retinal Ganglion Cells/pathology*
  20. Din NM, Taylor SR, Isa H, Tomkins-Netzer O, Bar A, Talat L, et al.
    JAMA Ophthalmol, 2014 Jul;132(7):859-65.
    PMID: 24789528 DOI: 10.1001/jamaophthalmol.2014.404
    IMPORTANCE: Uveitic glaucoma is among the most common causes of irreversible visual loss in uveitis. However, glaucoma detection can be obscured by inflammatory changes.

    OBJECTIVE: To determine whether retinal nerve fiber layer (RNFL) measurement can be used to detect glaucoma in uveitic eyes with elevated intraocular pressure (IOP).

    DESIGN, SETTING, AND PARTICIPANTS: Comparative case series of RNFL measurement using optical coherence tomography performed from May 1, 2010, through October 31, 2012, at a tertiary referral center. We assigned 536 eyes with uveitis (309 patients) in the following groups: normal contralateral eyes with unilateral uveitis (n = 72), normotensive uveitis (Uv-N) (n = 143), raised IOP and normal optic disc and/or visual field (Uv-H) (n = 233), and raised IOP and glaucomatous disc and/or visual field (Uv-G) (n = 88).

    EXPOSURES: Eyes with uveitis and elevated IOP (>21 mm Hg) on at least 2 occasions.

    MAIN OUTCOMES AND MEASURES: Comparison of RNFL values between groups of eyes and correlation with clinical data; risk factors for raised IOP, glaucoma, and RNFL thinning.

    RESULTS: Mean (SD) global RNFL was thicker in Uv-N (106.4 [21.4] µm) compared with control (96.0 [9.0] µm; P 

    Matched MeSH terms: Retinal Ganglion Cells/pathology*
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