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| 1 | Magnesium acetyltaurate prevents retinal damage and visual impairment in rats through suppression of NMDA-induced upregulation of NF-κB,p53 and AP-1(c-Jun/c-Fos)显示文摘Magnesium acetyltaurate(MgAT)has been shown to have a protective effect against N-methyl-D-aspartate(NMDA)-induced retinal cell apoptosis.The current study investigated the involvement of nuclear factor kappa-B(NF-κB),p53 and AP-1 family members(c-Jun/c-Fos)in neuroprotection by MgAT against NMDA-induced retinal damage.In this study,Sprague-Dawley rats were randomized to undergo intravitreal injection of vehicle,NMDA or MgAT as pre-treatment to NMDA.Seven days after injections,retinal ganglion cells survival was detected using retrograde labelling with fluorogold and BRN3A immunostaining.Functional outcome of retinal damage was assessed using electroretinography,and the mechanisms underlying antiapoptotic effect of MgAT were investigated through assessment of retinal gene expression of NF-κB,p53 and AP-1 family members(c-Jun/c-Fos)using reverse transcription-polymerase chain reaction.Retinal phospho-NF-κB,phospho-p53 and AP-1 levels were evaluated using western blot assay.Rat visual functions were evaluated using visual object recognition tests.Both retrograde labelling and BRN3A immunostaining revealed a significant increase in the number of retinal ganglion cells in rats receiving intravitreal injection of MgAT compared with the rats receiving intravitreal injection of NMDA.Electroretinography indicated that pre-treatment with MgAT partially preserved the functional activity of NMDA-exposed retinas.MgAT abolished NMDA-induced increase of retinal phospho-NF-κB,phospho-p53 and AP-1 expression and suppressed NMDA-induced transcriptional activity of NF-κB,p53 and AP-1 family members(c-Jun/c-Fos).Visual object recognition tests showed that MgAT reduced difficulties in recognizing the visual cues(i.e.objects with different shapes)after NMDA exposure,suggesting that visual functions of rats were relatively preserved by pre-treatment with MgAT.In conclusion,pre-treatment with MgAT prevents NMDA induced retinal injury by inhibiting NMDA-induced neuronal apoptosis via downregulation of transcriptional activity of NF-κB,p53 and AP-1-mediated c-Jun/c-Fos.The experiments were approved by the Animal Ethics Committee of Universiti Teknologi MARA(UiTM),Malaysia,UiTM CARE No 118/2015 on December 4,2015 and UiTM CARE No 220/7/2017 on December 8,2017 and Ethics Committee of Belgorod State National Research University,Russia,No 02/20 on January 10,2020. | Lidawani Lambuk Igor Iezhitsa Renu Agarwal Puneet Agarwal Anna Peresypkina Anna Pobeda Nafeeza Mohd Ismail | 2021 | Neural Regeneration Research2021，16，11： | 5 |
| 2 | Taurine protects against retinal and optic nerve damage induced by endothelin-1 in rats via antioxidant effects显示文摘Endothelin-1(ET-1), a potent vasoconstrictor, is involved in retinal vascular dysregulation and oxidative stress in glaucomatous eyes. Taurine(TAU), a naturally occurring free amino acid, is known for its neuroprotective and antioxidant properties. Hence, we evaluated its neuroprotective properties against ET-1 induced retinal and optic nerve damage. ET-1 was administered intravitreally to Sprague-Dawley rats and TAU was injected as pre-, co-or post-treatment. Animals were euthanized seven days post TAU injection. Retinae and optic nerve were examined for morphology, and were also processed for caspase-3 immunostaining. Retinal redox status was estimated by measuring retinal superoxide dismutase, catalase, glutathione, and malondialdehyde levels using enzyme-linked immuosorbent assay. Histopathological examination showed significantly improved retinal and optic nerve morphology in TAU-treated groups. Morphometric examination showed that TAU pre-treatment provided marked protection against ET-1 induced damage to retina and optic nerve. In accordance with the morphological observations, immunostaining for caspase showed a significantly lesser number of apoptotic retinal cells in the TAU pre-treatment group. The retinal oxidative stress was reduced in all TAU-treated groups, and particularly in the pre-treatment group. The findings suggest that treatment with TAU, particularly pre-treatment, prevents apoptosis of retinal cells induced by ET-1 and hence prevents the changes in the morphology of retina and optic nerve. The protective effect of TAU against ET-1 induced retinal and optic nerve damage is associated with reduced retinal oxidative stress. | Natasha Najwa Nor Arfuzir Renu Agarwal Igor Iezhitsa Puneet Agarwal Sabrilhakim Sidek Nafeeza Mohd Ismail | 2018 | Neural Regeneration Research2018，13，11： | 3 |
| 3 | A comparison between tocopherol and tocotrienol effects on gastric parameters in rats exposed to stress显示文摘 | Nafeeza MI Khalid BAK | 2005 | Asia Pacific Journal of Clinical Nutrition2005，14，4： | 1 |
| 4 | Phytonutrient:Effects on lipid peroxidation in experimental gastritis induced by restraint stress显示文摘 | Nur Azlina MF Nafeeza MI | | 0，，03： | 1 |
| 5 | Neuroprotective effects of exogenous brain-derived neurotrophic factor on amyloid-beta 1-40-induced retinal degeneration显示文摘Amyloid-beta(Aβ)-related alterations,similar to those found in the brains of patients with Alzheimer's disease,have been observed in the retina of patients with glaucoma.Decreased levels of brain-derived neurotrophic factor(BDNF)are believed to be associated with the neurotoxic effects of Aβpeptide.To investigate the mechanism underlying the neuroprotective effects of BDNF on Aβ_(1-40)-induced retinal injury in Sprague-Dawley rats,we treated rats by intravitreal administration of phosphate-buffered saline(control),Aβ_(1-40)(5 nM),or Aβ_(1-40)(5 nM)combined with BDNF(1μg/mL).We found that intravitreal administration of Aβ_(1-40)induced retinal ganglion cell apoptosis.Fluoro-Gold staining showed a significantly lower number of retinal ganglion cells in the Aβ_(1-40)group than in the control and BDNF groups.In the Aβ_(1-40)group,low number of RGCs was associated with increased caspase-3 expression and reduced TrkB and ERK1/2 expression.BDNF abolished Aβ_(1-40)-induced increase in the expression of caspase-3 at the gene and protein levels in the retina and upregulated TrkB and ERK1/2 expression.These findings suggest that treatment with BDNF prevents RGC apoptosis induced by Aβ_(1-40)by activating the BDNF-TrkB signaling pathway in rats. | Mohd Aizuddin Mohd Lazaldin Igor Iezhitsa Renu Agarwal Puneet Agarwal Nafeeza Mohd Ismail | 2023 | Neural Regeneration Research2023，18，2： | 1 |
| 6 | Nanoscale drug delivery systems and the blood - brain barrier 显示文摘 | ALYAUTDIN R KHALIN I NAFEEZA M I | 2014 | Int J Nanomedicine2014，9，： | 1 |
| 7 | Nanoscale drug delivery systems and the blood-brain barrier 显示文摘 | Alyautdin R Khalin I Nafeeza M I | 2014 | hat J Nanomedicine2014，9，： | 1 |
| 8 | The effects of palm vitamin E on stress hormone levels and gastric lesions in stress-induced rats显示文摘 | Aziz Ibrahim IA Kamisah Y Nafeeza MI | 2012 | Arch Med Sci2012，8，1： | 1 |
| 9 | Nanoscale drug delivery systems and the blood-brain barrier显示文摘 | Alyautdin R Khalin I Nafeeza MI | 2014 | Int J Nanomedicine2014，9，： | 1 |
| 10 | Dose-dependent effects of NMDA on retinal and optic nerve morphology in rats显示文摘AIM: To investigate dose-dependent effects of N-methylD-aspartate(NMDA) on retinal and optic nerve morphology in rats.METHODS: Sprague Dawley rats, 180-250 g in weight were divided into four groups. Groups 1, 2, 3 and 4 were intravitreally administered with vehicle and NMDA at the doses 80, 160 and 320 nmol respectively. Seven days after injection, rats were euthanized, and their eyes were taken for optic nerve toluidine blue and retinal hematoxylin and eosin stainings. The TUNEL assay was done for detecting apoptotic cells.RESULTS: All groups treated with NMDA showed significantly reduced ganglion cell layer(GCL) thickness within inner retina, as compared to control group. Group NMDA 160 nmol showed a significantly greater GCL thickness than the group NMDA 320 nmol. Administration of NMDA also resulted in a dose-dependent decrease in the number of nuclei both per 100 μm GCL length and per 100 μm2 of GCL. Intravitreal NMDA injection caused dosedependent damage to the optic nerve. The degeneration of nerve fibres with increased clearing of cytoplasm was observed more prominently as the NMDA dose increased. In accordance with the results of retinal morphometry analysis and optic nerve grading, TUNEL staining demonstrated NMDA-induced excitotoxic retinal injury in a dose-dependent manner.CONCLUSION: Our results demonstrate dose-dependent effects of NMDA on retinal and optic nerve morphology in rats that may be attributed to differences in the severity of excitotoxicity and oxidative stress. Our results also suggest that care should be taken while making dose selections experimentally so that the choice might best uphold study objectives. | Lidawani Lambuk Azliana Jusnida Ahmad Jafri Igor Iezhitsa Renu Agarwal Nor Salmah Bakar Puneet Agarwal Aimy Abdullah Nafeeza Mohd Ismail | 2019 | International Journal of Ophthalmology(English edition)2019，12，5： | 0 |
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