Oxidative stress accelerates synaptic glutamate dyshomeostasis and NMDARs disorder during methylmercury‐induced neuronal apoptosis in rat cerebral cortex

2020 ◽  
Vol 35 (6) ◽  
pp. 683-696 ◽  
Author(s):  
Tianyao Yang ◽  
Zhaofa Xu ◽  
Wei Liu ◽  
Bin Xu ◽  
Yu Deng
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Neuronal Apoptosis ◽  
Rat Cerebral Cortex

scholarly journals Sleep disruption elevates oxidative stress in parvalbumin-positive cells of the rat cerebral cortex

SLEEP ◽  
2018 ◽  
Vol 42 (1) ◽  
Author(s):  
John H Harkness ◽  
Priyanka N Bushana ◽  
Ryan P Todd ◽  
William C Clegern ◽  
Barbara A Sorg ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Rat Cerebral Cortex ◽  
Sleep Disruption

scholarly journals Neuroprotective Effect of Physical Exercise on Neuronal Apoptosis Induced by Tramadol in Cerebral Cortex of Rats

2020 ◽  
Vol 10 (6) ◽  
pp. 7209-7222
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Physical Exercise ◽  
Cortical Neurons ◽  
Neuronal Apoptosis ◽  
Neuroprotective Effect ◽  
Physiological Saline ◽  
Male Rats ◽  
Control Group ◽  
Oxidative Stress Biomarkers

Tramadol is a centrally acting analgesic agent with low affinity for opioid receptors, used for treating moderate to severe pain. Tramadol, like other opioids, induces neuronal apoptosis, which causes multiple neuronal impairments. The current study was conducted to evaluate the potential neuroprotective role of physical exercises on tramadol-induced neuronal apoptosis in the cerebral cortex of rats. Thirty adult male rats were divided into three groups (n= 10) as follow; the control group was gavaged with physiological saline (0.9% NaCl); tramadol group was daily administered with tramadol (40 mg/kg) for 28 days, and physical exercise group was administered with the same dose as tramadol group, then rats were forced to run on the treadmill for 30 min, once a day for 28 days. Tramadol induced histopathological changes in the form of neuroses degeneration and apoptosis. These findings were confirmed by immunohistochemical and blotting studies, which showed upregulation of p53 and downregulation of Bcl-2. In addition, malondialdehyde (MDA), myeloperoxidase (MPO), and nuclear factor kappa B (NF-κB) significantly increased following tramadol administration. At the same time, glutathione (GSH) and glutathione peroxidase (GPx) were decreased. In contrast, physical exercise was found to protect cortical neurons from degeneration and apoptosis produced by tramadol. This was evidenced by the downregulation of p53 and upregulating Bcl-2 expression and the improved changes in the oxidative stress biomarkers in rats. Physical exercise reduced the neuronal apoptosis and degeneration in the cerebral cortex following tramadol administration through suppressing oxidative stress.

The effects of mTOR or Vps34-mediated autophagy on methylmercury-induced neuronal apoptosis in rat cerebral cortex

2021 ◽  
pp. 112386
Author(s):  
Linlin Ni ◽  
Yanfeng Wei ◽  
Jingjing Pan ◽  
Xiaoyang Li ◽  
Bin Xu ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Neuronal Apoptosis ◽  
Rat Cerebral Cortex
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