scholarly journals Neuroprotective Effects of Transcription Factor Brn3b in an Ocular Hypertension Rat Model of Glaucoma

2015 ◽  
Vol 56 (2) ◽  
pp. 893-907 ◽  
Author(s):  
D. L. Stankowska ◽  
A. Z. Minton ◽  
M. A. Rutledge ◽  
B. H. Mueller ◽  
N. R. Phatak ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Ocular Hypertension ◽  
Rat Model ◽  
Neuroprotective Effects

scholarly journals Neuroprotective Effect of Statins in a Rat Model of Chronic Ocular Hypertension

2021 ◽  
Vol 22 (22) ◽  
pp. 12500
Author(s):  
Mi-Lyang Kim ◽  
Kyung Rim Sung ◽  
Junki Kwon ◽  
Go Woon Choi ◽  
Jin A Shin
Keyword(s):  
Ocular Hypertension ◽  
Rat Model ◽  
Ganglion Cells ◽  
Neuroprotective Effect ◽  
Statin Treatment ◽  
Glial Activation ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Hematoxylin And Eosin ◽  
Glaucoma Treatment

Glaucoma is an optic neuropathy in which the degeneration of retinal ganglion cells (RGCs) results in irreversible vison loss. Therefore, neuroprotection of RGCs from glaucomatous afflictions is crucial for glaucoma treatment. In this study, we aimed to investigate the beneficial effects of statins in the protection of RGCs using a rat model. Glaucomatous injury was induced in rats by chronic ocular hypertension (OHT) achieved after performing a circumlimbal suture. The rats were given either statins such as simvastatin and atorvastatin or a solvent weekly for 6 weeks. Retina sections underwent hematoxylin and eosin, Brn3a, or cleaved casepase-3 staining to evaluate RGC survival. In addition, modulation of glial activation was assessed. While the retinas without statin treatment exhibited increased RGC death due to chronic OHT, statins promoted the survival of RGCs and reduced apoptosis. Statins also suppressed chronic OHT-mediated glial activation in the retina. Our results demonstrate that statins exert neuroprotective effects in rat retinas exposed to chronic OHT, which may support the prospect of statins being a glaucoma treatment.

scholarly journals Platelet-Derived Growth Factor Preserves Retinal Synapses in a Rat Model of Ocular Hypertension

2016 ◽  
Vol 57 (3) ◽  
pp. 842 ◽  
Author(s):  
Rachel S. Chong ◽  
Andrew Osborne ◽  
Raquel Conceição ◽  
Keith R. Martin
Keyword(s):  
Growth Factor ◽  
Ocular Hypertension ◽  
Rat Model ◽  
Platelet Derived Growth Factor

scholarly journals Functional Recovery after Scutellarin Treatment in Transient Cerebral Ischemic Rats: A Pilot Study with18F-Fluorodeoxyglucose MicroPET

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Jin-hui Li ◽  
Jing Lu ◽  
Hong Zhang
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Neurological Deficit ◽  
Neuronal Maturation ◽  
Vascular Density ◽  
Sham Operation ◽  
Therapeutic Effects ◽  
Neuroprotective Effects ◽  
Neuronal Marker ◽  
Cerebral Ischemic

Objective. To investigate neuroprotective effects of scutellarin (Scu) in a rat model of cerebral ischemia with use of18F-fluorodeoxyglucose (18F-FDG) micro positron emission tomography (microPET).Method. Middle cerebral artery occlusion was used to establish cerebral ischemia. Rats were divided into 5 groups: sham operation, cerebral ischemia-reperfusion untreated (CIRU) group, Scu-25 group (Scu 25 mg/kg/d), Scu-50 group (Scu 50 mg/kg/d), and nimodipine (10 mg/Kg/d). The treatment groups were given for 2 weeks. The therapeutic effects in terms of cerebral infarct volume, neurological deficit scores, and cerebral glucose metabolism were evaluated. Levels of vascular density factor (vWF), glial marker (GFAP), and mature neuronal marker (NeuN) were assessed by immunohistochemistry.Results. The neurological deficit scores were significantly decreased in the Scu-50 group compared to the CIRU group (P<0.001).18F-FDG accumulation in the ipsilateral cerebral infarction increased steadily over time in Scu-50 group compared with CIRU group (P<0.01) and Scu-25 group (P<0.01). Immunohistochemical analysis demonstrated Scu-50 enhanced neuronal maturation.Conclusion.18F-FDG microPET imaging demonstrated metabolic recovery after Scu-50 treatment in the rat model of cerebral ischemia. The neuroprotective effects of Scu on cerebral ischemic injury might be associated with increased regional glucose activity and neuronal maturation.

Conifer Essential Oils Reversed Amyloid Beta1-42 Action by Modulating BDNF and ARC Expression in The Rat Hippocampus

2021 ◽  
Vol 20 ◽  
Author(s):  
Paula Alexandra Postu ◽  
Adrian Tiron ◽  
Crina Elena Tiron ◽  
Dragoș Lucian Gorgan ◽  
Marius Mihasan ◽  
...  
Keyword(s):  
Essential Oils ◽  
Dna Fragmentation ◽  
Rat Model ◽  
Pinus Halepensis ◽  
Chemical Constituents ◽  
Gene Expressions ◽  
Bdnf Expression ◽  
Neuroprotective Effects ◽  
Positive Effects ◽  
Cognitive Improvement

Background: The conifer species Pinus halepensis (Pinaceae) and Tetraclinis articulata (Cupressaceae) are widely used in traditional medicine due to their health beneficial properties. Objective: This study aimed to investigate the mechanisms by which P. halepensis and T. articulata essential oils (1% and 3%) could exhibit neuroprotective effects in an Alzheimer's disease (AD) rat model, induced by intracerebroventricular (i.c.v.) administration of amyloid beta1-42 (Aβ1-42). Method: The essential oils were administered by inhalation to the AD rat model, once daily, for 21 days. DNA fragmentation was assessed through Cell Death Detection ELISA kit. Brain-derived neurotrophic factor (BDNF), activity-regulated cytoskeleton-associated protein (ARC) and interleukin-1β (IL-1β) gene expressions were determined by RT-qPCR analysis, while BDNF and ARC protein expressions were assessed using immunohistochemistry technique. Results: Our data showed that both essential oils substantially attenuated memory impairments, with P. halepensis mainly stimulating ARC expression and T. articulata mostly enhancing BDNF expression. Also, the inhalation of essential oils reduced IL-1β expression and induced positive effects against DNA fragmentation associated with Aβ1-42-induced toxicity, further contributing to the cognitive improvement in the rats with AD-like model. Conclusion: Our findings provide further evidence that these essential oils and their chemical constituents could be natural agents of therapeutic interest against Aβ1-42-induced neurotoxicity.

scholarly journals Neuroprotective Effects of Mitochondria-Targeted Plastoquinone and Thymoquinone in a Rat Model of Brain Ischemia/Reperfusion Injury

Molecules ◽  
2015 ◽  
Vol 20 (8) ◽  
pp. 14487-14503 ◽  
Author(s):  
Denis Silachev ◽  
Egor Plotnikov ◽  
Ljubava Zorova ◽  
Irina Pevzner ◽  
Natalia Sumbatyan ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Brain Ischemia ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neuroprotective Effects

Neuroprotective Effects of Paeoniflorin on 6-OHDA-Lesioned Rat Model of Parkinson’s Disease

2016 ◽  
Vol 41 (11) ◽  
pp. 2923-2936 ◽  
Author(s):  
Xiao-Su Gu ◽  
Fen Wang ◽  
Cai-Yi Zhang ◽  
Cheng-Jie Mao ◽  
Jing Yang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Neuroprotective Effects

scholarly journals Nurr1 modulation mediates neuroprotective effects of statins

2021 ◽  
Author(s):  
Sabine Willems ◽  
Whitney Kilu ◽  
Giuseppe Faudone ◽  
Jan Heering ◽  
Daniel Merk
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Gene Expression Analysis ◽  
Energy Utilization ◽  
Neuroprotective Effects ◽  
Simvastatin Treatment ◽  
Differential Gene Expression Analysis ◽  
Functional Studies ◽  
Promising Therapeutic Target ◽  
Differential Gene

AbstractThe ligand-sensing transcription factor Nurr1 emerges as a promising therapeutic target for neurodegenerative pathologies but Nurr1 ligands for functional studies and therapeutic validation are lacking. Here we report pronounced Nurr1 modulation by statins for which clinically relevant neuroprotective effects have been demonstrated. Several statins directly affected Nurr1 activity in cellular and cell-free settings with low micromolar to sub-micromolar potencies. Simvastatin exhibited anti-inflammatory effects in astrocytes which were abrogated by Nurr1 knockdown. Differential gene expression analysis in native and Nurr1 silenced cells revealed strong proinflammatory effects of Nurr1 knockdown while simvastatin treatment induced several neuroprotective mechanisms via Nurr1, for example, in energy utilization and reduced apoptosis. These findings suggest Nurr1 involvement in the well-documented but mechanistically elusive neuroprotection by statins.

Possible Neuroprotective Effects of Magnesium Sulfate and Melatonin as Both Pre- and Post-Treatment in a Neonatal Hypoxic-Ischemic Rat Model

Neonatology ◽  
2011 ◽  
Vol 99 (4) ◽  
pp. 302-310 ◽  
Author(s):  
Merih Cetinkaya ◽  
Tülin Alkan ◽  
Fadil Ozyener ◽  
Ilker Mustafa Kafa ◽  
Mustafa Ayberk Kurt ◽  
...  
Keyword(s):  
Magnesium Sulfate ◽  
Rat Model ◽  
Post Treatment ◽  
Neuroprotective Effects
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