Neuroprotective effects of SNX-185 in an In Vitro model of TBI with a second insult

2013 ◽  
Vol 31 (2) ◽  
pp. 141-153 ◽  
Author(s):  
Kiarash Shahlaie ◽  
Gene G. Gurkoff ◽  
Bruce G. Lyeth ◽  
J. Paul Muizelaar ◽  
Robert F. Berman
Keyword(s):  
In Vitro Model ◽  
Neuroprotective Effects ◽  
Vitro Model

scholarly journals Delivery of Thyronamines (TAMs) to the Brain: A Preliminary Study

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1616
Author(s):  
Nicoletta di Leo ◽  
Stefania Moscato ◽  
Marco Borso' ◽  
Simona Sestito ◽  
Beatrice Polini ◽  
...  
Keyword(s):  
High Performance ◽  
In Vitro Model ◽  
New Drugs ◽  
Therapeutic Approaches ◽  
Neuroprotective Effects ◽  
Pharmacological Response ◽  
Preliminary Study ◽  
Vitro Model ◽  
The Brain

Recent reports highlighted the significant neuroprotective effects of thyronamines (TAMs), a class of endogenous thyroid hormone derivatives. In particular, 3-iodothyronamine (T1AM) has been shown to play a pleiotropic role in neurodegeneration by modulating energy metabolism and neurological functions in mice. However, the pharmacological response to T1AM might be influenced by tissue metabolism, which is known to convert T1AM into its catabolite 3-iodothyroacetic acid (TA1). Currently, several research groups are investigating the pharmacological effects of T1AM systemic administration in the search of novel therapeutic approaches for the treatment of interlinked pathologies, such as metabolic and neurodegenerative diseases (NDDs). A critical aspect in the development of new drugs for NDDs is to know their distribution in the brain, which is fundamentally related to their ability to cross the blood–brain barrier (BBB). To this end, in the present study we used the immortalized mouse brain endothelial cell line bEnd.3 to develop an in vitro model of BBB and evaluate T1AM and TA1 permeability. Both drugs, administered at 1 µM dose, were assayed by high-performance liquid chromatography coupled to mass spectrometry. Our results indicate that T1AM is able to efficiently cross the BBB, whereas TA1 is almost completely devoid of this property.

The Blockade of K+‐ATP Channels has Neuroprotective Effects in an In Vitro Model of Brain Ischemia

2007 ◽  
pp. 383-395 ◽  
Author(s):  
Robert Nisticò ◽  
Silvia Piccirilli ◽  
L. Sebastianelli ◽  
Giuseppe Nisticò ◽  
G. Bernardi ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
In Vitro Model ◽  
Neuroprotective Effects ◽  
Vitro Model

Neuroprotective effects of dexmedetomidine conditioning strategies: Evidences from an in vitro model of cerebral ischemia

Life Sciences ◽  
2016 ◽  
Vol 144 ◽  
pp. 162-169 ◽  
Author(s):  
Raquel Rodríguez-González ◽  
Tomás Sobrino ◽  
Sonia Veiga ◽  
Pablo López ◽  
Javier Rodríguez-García ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
In Vitro Model ◽  
Neuroprotective Effects ◽  
Vitro Model

Neuroprotective effects of riluzole: An electrophysiological and histological analysis in an in vitro model of ischemia

Synapse ◽  
1999 ◽  
Vol 32 (3) ◽  
pp. 147-152 ◽  
Author(s):  
Antonio Siniscalchi ◽  
Cristina Zona ◽  
Giuseppe Sancesario ◽  
Enza D'Angelo ◽  
Yong Chun Zeng ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Histological Analysis ◽  
Neuroprotective Effects ◽  
Vitro Model

scholarly journals The Moringin/α-CD Pretreatment Induces Neuroprotection in an In Vitro Model of Alzheimer’s Disease: A Transcriptomic Study

2021 ◽  
Vol 43 (1) ◽  
pp. 197-214
Author(s):  
Serena Silvestro ◽  
Luigi Chiricosta ◽  
Agnese Gugliandolo ◽  
Renato Iori ◽  
Patrick Rollin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
In Vitro Model ◽  
Neurodegenerative Disorder ◽  
Senile Dementia ◽  
Neuroprotective Effects ◽  
Model Of Alzheimer’S Disease ◽  
Vitro Model ◽  
Ad Prevention

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and represents the most common form of senile dementia. Autophagy and mitophagy are cellular processes that play a key role in the aggregation of β-amyloid (Aβ) and tau phosphorylation. As a consequence, impairment of these processes leads to the progression of AD. Thus, interest is growing in the search for new natural compounds, such as Moringin (MOR), with neuroprotective, anti-amyloidogenic, antioxidative, and anti-inflammatory properties that could be used for AD prevention. However, MOR appears to be poorly soluble and stable in water. To increase its solubility MOR was conjugated with α-cyclodextrin (MOR/α-CD). In this work, it was evaluated if MOR/α-CD pretreatment was able to exert neuroprotective effects in an AD in vitro model through the evaluation of the transcriptional profile by next-generation sequencing (NGS). To induce the AD model, retinoic acid-differentiated SH-SY5Y cells were exposed to Aβ1-42. The MOR/α-CD pretreatment reduced the expression of the genes which encode proteins involved in senescence, autophagy, and mitophagy processes. Additionally, MOR/α-CD was able to induce neuronal remodeling modulating the axon guidance, principally downregulating the Slit/Robo signaling pathway. Noteworthy, MOR/α-CD, modulating these important pathways, may induce neuronal protection against Aβ1-42 toxicity as demonstrated also by the reduction of cleaved caspase 3. These data indicated that MOR/α-CD could attenuate the progression of the disease and promote neuronal repair.

Neuroprotective effects of propofol in an in vitro model of cerebral ischemia

2004 ◽  
Vol 21 (Supplement 32) ◽  
pp. 90
Author(s):  
C. Adembri ◽  
E. Gramigni ◽  
L. Venturi ◽  
A. Chiarugi ◽  
A. R. De Gaudio ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
In Vitro Model ◽  
Neuroprotective Effects ◽  
Vitro Model
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