Neuroprotective Action of Deer Bone Extract Against Glutamate or Aβ1–42-Induced Oxidative Stress in Mouse Hippocampal Cells

2014 ◽  
Vol 17 (2) ◽  
pp. 226-235 ◽  
Author(s):  
Cho Rong Kim ◽  
Hye Lyun Jeon ◽  
Suk Kyung Shin ◽  
Hyun Jeong Kim ◽  
Chang-Won Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroprotective Action

scholarly journals Neuroprotective Effect of the Ginsenoside Rg1 on Cerebral Ischemic Injury In Vivo and In Vitro Is Mediated by PPARγ-Regulated Antioxidative and Anti-Inflammatory Pathways

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yang Li ◽  
Yue Guan ◽  
Ying Wang ◽  
Chun-Lei Yu ◽  
Feng-Guo Zhai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Ginsenoside Rg1 ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Cerebral Ischemic ◽  
Neuroprotective Action

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.

Propofol, an anesthetic possessing neuroprotective action against oxidative stress, promotes the process of cell death induced by H2O2 in rat thymocytes

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

scholarly journals From Neuroinflammation to Neuroprotection: Focus on Potential New Therapeutic Targets in Cognitive Impairment

2020 ◽  
pp. 1-4
Author(s):  
Pietro Gareri ◽  
Antonino Maria Cotroneo ◽  
Pietro Gareri ◽  
Valeria Graziella Laura Manfredi
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Activation ◽  
Scientific Evidence ◽  
Neuronal Cell ◽  
Cholinergic Neuron ◽  
Oxygen Species ◽  
Cell Energy ◽  
Neuroprotective Action

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.

scholarly journals Neuroprotective Action of Multitarget 7-Aminophenanthridin-6(5H)-one Derivatives against Metal-Induced Cell Death and Oxidative Stress in SN56 Cells

2021 ◽  
Author(s):  
Paula Moyano ◽  
David Vicente-Zurdo ◽  
Cristina Blázquez-Barbadillo ◽  
J. Carlos Menéndez ◽  
Juan F. González ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
And Oxidative Stress ◽  
Neuroprotective Action

Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp (Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Secondary Metabolites ◽  
Human Health ◽  
Grass Carp ◽  
Aquatic Environment ◽  
Ctenopharyngodon Idellus

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.

Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov
Keyword(s):  
Oxidative Stress ◽  
Head And Neck ◽  
Transcriptional Activation ◽  
Platinum Resistance ◽  
Mrna Levels ◽  
Strong Positive Correlation ◽  
Platinum Compounds ◽  
Copper Chelation ◽  
Novel Approach ◽  
Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

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