scholarly journals Nitroxide radical-containing redox nanoparticles protect neuroblastoma SH-SY5Y cells against 6-hydroxydopamine toxicity

2021 ◽  
Vol 177 ◽  
pp. S71
Author(s):  
Monika Pichla ◽  
Łukasz Pułaski ◽  
Katarzyna D. Kania ◽  
Ireneusz Stefaniuk ◽  
Bogumił Cieniek ◽  
...  
1976 ◽  
Vol 17 (3) ◽  
pp. 419-419 ◽  
Author(s):  
Masayori OZAKI ◽  
Kazunobu SUGAWARA ◽  
Naoko TAKAMI ◽  
Masashi OGAWA ◽  
Masami NIWA

2020 ◽  
Vol 20 (10) ◽  
pp. 1560-1568 ◽  
Author(s):  
Yan-Qiu Wang ◽  
Yi-Bing Chen ◽  
Dong Xu ◽  
Yuan-Lu Cui

Objective: Energy metabolism disorder is one of the causes of Parkinson's disease (PD). Rodents, such as rats and mice are often used to establish animal models of PD. This paper used a bibliometric method to analyze the studies of rat and mouse PD models published between 2009 and 2018 in the Web of Science (WOS) database using CiteSpace V software. In addition, we conducted a literature review on the development status and research hotspots in this field in the past ten years. Methods: The related articles on rat and mouse PD models were retrieved from the WOS database, and an analysis of the keywords in these articles was conducted using CiteSpace V. A timeline graph was developed by the software in order to show the focus of researchers in the PD field. Results : A total of 8,636 articles were obtained. Results of the cluster analysis in the PD field such as neuroinflammation, oxidative stress, and autophagy, contributed to the systematic review about the pathogenesis of PD. At the same time, based on the property of the model drug, this review has summarized and compared different administration techniques and mechanisms of 6-hydroxydopamine (6- OHDA), 1-methyl-4-phenyl-1, 2, 4, 5-tetrahydropyridine (MPTP), paraquat and rotenone. Conclusion: According to the bibliometric analysis, studies on PD were focused on the mechanisms of oxidative stress, neuroinflammation, and autophagy. Activated microglia releases inflammatory cytokines; mitochondrial dysfunction is caused by oxidative damage of mitochondrial protein; abnormal autophagy-lysosome pathway can lead to abnormal protein deposition in dopaminergic neurons. In addition, although many animal models of PD have been established, there are some limitations of such models. Therefore, it is necessary to develop models that accurately mimic human PD.


2021 ◽  
Vol 406 ◽  
pp. 113226
Author(s):  
Talita Tuon ◽  
Sandra S. Meirelles ◽  
Airam B. de Moura ◽  
Thayse Rosa ◽  
Laura A. Borba ◽  
...  

2021 ◽  
pp. 1-24
Author(s):  
Juho-Matti Renko ◽  
Arun Kumar Mahato ◽  
Tanel Visnapuu ◽  
Konsta Valkonen ◽  
Mati Karelson ◽  
...  

Background: Parkinson’s disease (PD) is a progressive neurological disorder where loss of dopamine neurons in the substantia nigra and dopamine depletion in the striatum cause characteristic motor symptoms. Currently, no treatment is able to halt the progression of PD. Glial cell line-derived neurotrophic factor (GDNF) rescues degenerating dopamine neurons both in vitro and in animal models of PD. When tested in PD patients, however, the outcomes from intracranial GDNF infusion paradigms have been inconclusive, mainly due to poor pharmacokinetic properties. Objective: We have developed drug-like small molecules, named BT compounds that activate signaling through GDNF’s receptor, the transmembrane receptor tyrosine kinase RET, both in vitro and in vivo and are able to penetrate through the blood-brain barrier. Here we evaluated the properties of BT44, a second generation RET agonist, in immortalized cells, dopamine neurons and rat 6-hydroxydopamine model of PD. Methods: We used biochemical, immunohistochemical and behavioral methods to evaluate the effects of BT44 on dopamine system in vitro and in vivo. Results: BT44 selectively activated RET and intracellular pro-survival AKT and MAPK signaling pathways in immortalized cells. In primary midbrain dopamine neurons cultured in serum-deprived conditions, BT44 promoted the survival of the neurons derived from wild-type, but not from RET knockout mice. BT44 also protected cultured wild-type dopamine neurons from MPP +-induced toxicity. In a rat 6-hydroxydopamine model of PD, BT44 reduced motor imbalance and could have protected dopaminergic fibers in the striatum. Conclusion: BT44 holds potential for further development into a novel, possibly disease-modifying therapy for PD.


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