scholarly journals New PAR1 Agonist Peptide Demonstrates Protective Action in a Mouse Model of Photothrombosis-Induced Brain Ischemia

2020 ◽  
Vol 14 ◽  
Author(s):  
Maksim Galkov ◽  
Ekaterina Kiseleva ◽  
Mikhail Gulyaev ◽  
Maria Sidorova ◽  
Liubov Gorbacheva
Keyword(s):  
Mouse Model ◽  
Brain Ischemia ◽  
Protective Action ◽  
Agonist Peptide

scholarly journals Reply to a Comment Paper on the Published Paper by Canta, A. et al: “Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity”—Antioxidants 2020, 9, 594

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 807
Author(s):  
Annalisa Canta ◽  
Alessia Chiorazzi ◽  
Eleonora Pozzi ◽  
Giulia Fumagalli ◽  
Laura Monza ◽  
...  
Keyword(s):  
Mouse Model ◽  
Nerve Fiber ◽  
Protective Action ◽  
Mechanisms Of Action ◽  
Nerve Fibers ◽  
Peripheral Neurotoxicity ◽  
Published Paper ◽  
Intraepidermal Nerve Fiber

The comments sent by Stehr, Lundstom and Karlsson with reference to our article “Calmangafodipir reduces sensory alterations and prevents intraepidermal nerve fiber loss in a mouse model of oxaliplatin-induced peripheral neurotoxicity“ are very interesting, since they suggest possible mechanisms of action of the compound, which might contribute to its protective action [...]

NAD+ administration decreases ischemic brain damage partially by blocking autophagy in a mouse model of brain ischemia

2012 ◽  
Vol 512 (2) ◽  
pp. 67-71 ◽  
Author(s):  
Chaobo Zheng ◽  
Jin Han ◽  
Weiliang Xia ◽  
Shengtao Shi ◽  
Jianrong Liu ◽  
...  
Keyword(s):  
Mouse Model ◽  
Brain Damage ◽  
Brain Ischemia ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

Mechanism of Tau Hyperphosphorylation Involving Lysosomal Enzyme Asparagine Endopeptidase in a Mouse Model of Brain Ischemia

2018 ◽  
Vol 63 (2) ◽  
pp. 821-833 ◽  
Author(s):  
Gustavo Basurto-Islas ◽  
Jin-hua Gu ◽  
Yunn Chyn Tung ◽  
Fei Liu ◽  
Khalid Iqbal
Keyword(s):  
Mouse Model ◽  
Brain Ischemia ◽  
Lysosomal Enzyme ◽  
Tau Hyperphosphorylation

scholarly journals UV light suppression of EAE (a mouse model of multiple sclerosis) is independent of vitamin D and its receptor

2019 ◽  
Vol 116 (45) ◽  
pp. 22552-22555 ◽  
Author(s):  
Amy A. Irving ◽  
Steven J. Marling ◽  
Jeremy Seeman ◽  
Lori A. Plum ◽  
Hector F. DeLuca
Keyword(s):  
Multiple Sclerosis ◽  
Vitamin D ◽  
Mouse Model ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Uv Light ◽  
Protective Action ◽  
Ultra Violet ◽  
Uv Exposure ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

Vitamin D and sunlight have each been reported to protect against the development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). To date, the contribution of each has been unclear as ultra violet (UV) exposure also causes the generation of vitamin D in the skin. To examine whether the UV based suppression of EAE results, at least, in part from the production of vitamin D, we studied the effect of UV light on EAE in mice unable to produce 7-dehydroxycholesterol (7-DHC), the required precursor of vitamin D. Furthermore, we examined UV suppression of EAE in mice devoid of the vitamin D receptor (VDR). Our results demonstrate that UV light suppression of EAE occurs in the absence of vitamin D production and in the absence of VDR. Future investigations will focus on identifying the pathway responsible for the protective action of UV in EAE and presumably human MS.

scholarly journals Upregulation of membrane‐bound metalloendopeptidase neurolysin in a mouse model of focal brain ischemia

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Mamoon Rashid ◽  
Li Yang ◽  
Thiruma V. Arumugam ◽  
Thomas J. Abbruscato ◽  
Vardan T. Karamyan
Keyword(s):  
Mouse Model ◽  
Brain Ischemia ◽  
Membrane Bound ◽  
Focal Brain Ischemia

Abstract WMP75: Development of a Theragnostic Probe for Stem Cell Tracking and Enhancing the Therapeutic Efficacy in a Mouse Model of Focal Ischemia

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Xiaojing Shi ◽  
Lu Zhang ◽  
Zhijun Zhang ◽  
Yongting Wang ◽  
Guo-Yuan Yang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Ischemic Stroke ◽  
Mouse Model ◽  
Cell Viability ◽  
Brain Ischemia ◽  
Therapeutic Efficacy ◽  
Cell Tracking ◽  
Photoacoustic Imaging

Objectives: Mesenchymal stem cell therapy has shown therapeutic potential for ischemic stroke. However, low cell viability and lack of multimodal imaging to track stem cell distribution limit its clinical translation. Here we developed a multifunctional probe to track stem cell viability and migration in a mouse model of focal brain ischemia. Methods: A theragnostic probe was developed by cobalt protoporphyrin IX (CoPP), with photoacoustic imaging detectability into 125 Iodine modified mesoporous silica nanoparticles ( 125 I-CoPP@MSN). The effect on cell viability and differentiation were examined in vitro . Adult male ICR mice (n=40) were subjected to 90 min transient middle cerebral artery occlusion. 125 I-CoPP@MSN labeled stem cells were transplanted into the peri-infarct region after 1 day of brain ischemia. Grafted cells was monitored by SPECT and photoacoustic imaging. The cell survival was evaluated by bioluminescence imaging. Results: 125 I-CoPP@MSNs have high efficiency for labeling cells without affecting their viability and differentiation. 125 I-CoPP@MSNs increased the viability of stem cells subjected to H 2 O 2 -induced oxidant stress in vitro , compared with controls ( p <0.05). Photoacoustic and SPECT imaging showed that 90±8% of graft cells were localized in the injection site and tended to migrate at 1 day after injection. The SPECT/CT signal started to decrease from 4 to 8 days. 125 I-CoPP@MSN labeling increased graft cell viability, reduced brain atrophy volume, and improved behavioral outcomes, compared to the controls ( p <0.05). Immunostaining results showed that the number of CD31 + and DCX + cells were increased in CoPP@MSN labeled group than that in controls (p<0.05). Conclusion: We conclude that 125 I-CoPP@MSNs is a novel probe for the real-time tracking and enhancing its therapeutic efficacy in ischemic stroke therapy.

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