Synthesis, characterization, and in vitro evaluation of new coordination complexes of platinum(ii) and rhenium(i) with a ligand targeting the translocator protein (TSPO)

2014 ◽  
Vol 43 (43) ◽  
pp. 16252-16264 ◽  
Author(s):  
Nicola Margiotta ◽  
Nunzio Denora ◽  
Sara Piccinonna ◽  
Valentino Laquintana ◽  
Francesco Massimo Lasorsa ◽  
...  

The 18 kDa translocator protein (TSPO) is overexpressed in many cancers and is also abundant in activated microglial cells occurring in neurodegenerative diseases.

Meta Gene ◽  
2018 ◽  
Vol 17 ◽  
pp. S22
Author(s):  
Yehor Pashkevych ◽  
Mariia Rudyk ◽  
Yevheniia Hurmach ◽  
Vitalina Svyatetska ◽  
Natalia Senchylo ◽  
...  

2019 ◽  
Vol 11 (6) ◽  
pp. 539-550 ◽  
Author(s):  
Thomas Kalina ◽  
Neydher Berroterán-Infante ◽  
Stefan Schmitl ◽  
Chrysoula Vraka ◽  
Marcus Hacker ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Sang Min Lee ◽  
Eun Jin Yang ◽  
Sun-Mi Choi ◽  
Seon Hwy Kim ◽  
Myung Gi Baek ◽  
...  

Bee venom (BV), which is extracted from honeybees, is used in traditional Korean medical therapy. Several groups have demonstrated the anti-inflammatory effects of BV in osteoarthritis bothin vivoandin vitro. Glutamate is the predominant excitatory neurotransmitter in the central nervous system (CNS). Changes in glutamate release and uptake due to alterations in the activity of glutamate transporters have been reported in many neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis. To assess if BV can prevent glutamate-mediated neurotoxicity, we examined cell viability and signal transduction in glutamate-treated neuronal and microglial cells in the presence and absence of BV. We induced glutamatergic toxicity in neuronal cells and microglial cells and found that BV protected against cell death. Furthermore, BV significantly inhibited the cellular toxicity of glutamate, and pretreatment with BV altered MAP kinase activation (e.g., JNK, ERK, and p38) following exposure to glutamate. These findings suggest that treatment with BV may be helpful in reducing glutamatergic cell toxicity in neurodegenerative diseases.


Author(s):  
Yue Jia ◽  
Dandan Zhang ◽  
Hua Yin ◽  
Haoran Li ◽  
Jing Du ◽  
...  

AbstractNeuroinflammation plays an important role in the onset and progression of neurodegenerative diseases. Microglia-mediated neuroinflammation have been proved to be the main reason for causing the neurodegenerative diseases. Ganoderic acid A (GAA), isolated from Ganoderma lucidum, showed anti-inflammatory effect in metabolism diseases. However, little research has been focused on the effect of GAA in neuroinflammation and the related mechanism. In the present study, lipopolysaccharide(LPS)-stimulated BV2 microglial cells were used to evaluate the anti-inflammatory capacity of GAA. Our data showed that GAA significantly suppressed LPS-induced BV2 microglial cells proliferation and activation in vitro. More strikingly, GAA promoted the conversion of BV2 microglial cells from M1 status induced by LPS to M2 status. Furthermore, GAA inhibited the pro-inflammatory cytokines release and promoted neurotrophic factor BDNF expression in LPS-induced BV2 microglial cells. Finally, we found that the expression of farnesoid-X-receptor (FXR) was prominently downregulated in LPS-stimulated BV2 microglial cells, antagonism of FXR with z-gugglesterone and FXR siRNA can reverse the effect of GAA in LPS-induced BV2 microglial cells. Taking together, our findings demonstrate that GAA can significantly inhibit LPS-induced neuroinflammation in BV2 microglial cells via activating FXR receptor.


2001 ◽  
Vol 120 (5) ◽  
pp. A316-A317
Author(s):  
P MAERTEN ◽  
S COLPAERT ◽  
Z LIU ◽  
K GEBOES ◽  
J CEUPPENS ◽  
...  

2006 ◽  
Vol 175 (4S) ◽  
pp. 18-18
Author(s):  
Kari Hendlin ◽  
Krishna Vedula ◽  
Christina Horn ◽  
Manoj Monga

Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
B Pinel ◽  
A Landreau ◽  
J Dubois ◽  
G Au do ◽  
F De la Poype ◽  
...  
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