Neuroprotective Action of Bilirubin against Oxidative Stress in Primary Hippocampal Cultures

1999 ◽  
Vol 890 (1 NEUROPROTECTI) ◽  
pp. 167-172 ◽  
Author(s):  
SYLVAIN DORE ◽  
SOLOMON H. SNYDER
2014 ◽  
Vol 17 (2) ◽  
pp. 226-235 ◽  
Author(s):  
Cho Rong Kim ◽  
Hye Lyun Jeon ◽  
Suk Kyung Shin ◽  
Hyun Jeong Kim ◽  
Chang-Won Ahn ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yang Li ◽  
Yue Guan ◽  
Ying Wang ◽  
Chun-Lei Yu ◽  
Feng-Guo Zhai ◽  
...  

The ginsenoside Rg1 exerts a neuroprotective effect during cerebral ischemia/reperfusion injury. Rg1 has been previously reported to improve PPARγexpression and signaling, consequently enhancing its regulatory processes. Due to PPARγ’s role in the suppression of oxidative stress and inflammation, Rg1’s PPARγ-normalizing capacity may play a role in the observed neuroprotective action of Rg1 during ischemic brain injury. We utilized a middle cerebral artery ischemia/reperfusion injury model in rats in addition to an oxygen glucose deprivation model in cortical neurons to elucidate the mechanisms underlying the neuroprotective effects of Rg1. We found that Rg1 significantly increased PPARγexpression and reduced multiple indicators of oxidative stress and inflammation. Ultimately, Rg1 treatment improved neurological function and diminished brain edema, indicating that Rg1 may exert its neuroprotective action on cerebral ischemia/reperfusion injury through the activation of PPARγsignaling. In addition, the present findings suggested that Rg1 was a potent PPARγagonist in that it upregulated PPARγexpression and was inhibited by GW9662, a selective PPARγantagonist. These findings expand our previous understanding of the molecular basis of the therapeutic action of Rg1 in cerebral ischemic injury, laying the ground work for expanded study and clinical optimization of the compound.


2006 ◽  
Vol 540 (1-3) ◽  
pp. 18-23 ◽  
Author(s):  
Ken-ichi Chikutei ◽  
Tomohiro M. Oyama ◽  
Shiro Ishida ◽  
Yoshiro Okano ◽  
Masako Kobayashi ◽  
...  

2020 ◽  
pp. 1-4
Author(s):  
Pietro Gareri ◽  
Antonino Maria Cotroneo ◽  
Pietro Gareri ◽  
Valeria Graziella Laura Manfredi

Neurodegeneration is closely linked to neuroinflammation. It is often associated with oxidative stress and meaningful changes in cell energy metabolism. Neuroinflammation is due to non-neuronal cell activation (microglia, astrocytes, mast cells) activation and proliferation. Also, it is associated with pro-inflammatory substances release, able to modify synaptic plasticity. Microglia and astrocytes activation lead to toxic agent’s release (reactive oxygen species, inflammatory cytokines); however, the final target of this process is the cholinergic neuron. A number of substances can promote neuroprotection; recent scientific evidence focuses on the role of sirtuins. In particular, SIRT1 is activated by caloric restriction, NAD biosynthesis and different activators, called STACs (Sirtuin Activating Compounds). Citicoline is one of the most powerful STACs. It has been widely shown to possess neuroprotective action, and lots of studies strengthened its possible role.


Glia ◽  
2009 ◽  
Vol 57 (3) ◽  
pp. 244-257 ◽  
Author(s):  
Takumi Fujita ◽  
Hidetoshi Tozaki-Saitoh ◽  
Kazuhide Inoue

Author(s):  
Paula Moyano ◽  
David Vicente-Zurdo ◽  
Cristina Blázquez-Barbadillo ◽  
J. Carlos Menéndez ◽  
Juan F. González ◽  
...  

2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.


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