scholarly journals Ethyl pyruvate prevents from chronic cerebral hypoperfusion via preserving cognitive function and decreasing oxidative stress, caspase 3 activation and IL-1β level

2018 ◽  
Vol 119 (08) ◽  
pp. 469-475 ◽  
Author(s):  
H. Sayan Ozacmak ◽  
V. H. Ozacmak ◽  
I. Turan
Author(s):  
Elaheh Ghasemi ◽  
Faezeh Afkhami Aghda ◽  
Mohammad Ebrahim Rezvani ◽  
Azadeh Shahrokhi Raeini ◽  
Zeynab Hafizibarjin ◽  
...  

AbstractBackgroundThe vascular changes due to cerebrovascular damage, especially on the capillaries, play a vital role in causing vascular dementia. Increasing oxidative stress can lead to tissue damage while reducing brain blood flow. The use of factors reducing the oxidative stress level can decrease the brain damages. Sulfur dioxide (SO2) is one of the most important air pollutants that lead to the development of severe brain damage in large quantities. However, studies have recently confirmed the protective effect of SO2 in cardiac ischemic injury, atherosclerosis and pulmonary infections.MethodsThe permanent bilateral common carotid artery occlusion (BCAO) method was used to induce chronic cerebral hypoperfusion (CCH). Two treatment groups of SO2 were studied. The animal cognitive performance was evaluated using the Morris water maze. Hippocampal tissue damage was examined after 2 months of BCAO. In the biochemical analysis, the activity of catalase and lipid peroxidation of the hippocampus was studied.ResultsNeuronal damage in hippocampus, as well as cognitive impairment in ischemia groups treated with SO2 showed a significant improvement. Catalase activity was also significantly increased in the hippocampus of treated groups.ConclusionsAccording to the results, SO2 is likely to be effective in reducing the CCH-caused damages by increasing the antioxidant capacity of the hippocampus.


Life Sciences ◽  
2012 ◽  
Vol 91 (1-2) ◽  
pp. 29-36 ◽  
Author(s):  
Fernanda Cechetti ◽  
Paulo Valdeci Worm ◽  
Gisele Lovatel ◽  
Felipe Moysés ◽  
Ionara Rodrigues Siqueira ◽  
...  

2017 ◽  
Vol 40 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Dandan Zhang ◽  
Yining Xiao ◽  
Peiyuan Lv ◽  
Zhenjie Teng ◽  
Yanhong Dong ◽  
...  

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Zikang Guo ◽  
Jiang Li

AbstractThe present investigation evaluates the neuroprotective effect of chlorogenic acid (CA) in alcohol-induced brain damage in neonatal rats. Ethanol (12 % v/v, 5 g/kg) was administered orally in the wistar rat pups on postnatal days (PD) 7-9. Chlorogenic acid (100 and 200 mg/kg, p.o.) was administered continuously from PD 6 to 28. Cognitive function was estimated by Morris water maze (MWM) test. However, activity of acetylcholinesterase, inflammatory mediators, parameters of oxidative stress and activity of caspase-3 enzyme was estimated in the tissue homogenate of cerebral cortex and hippocampus of ethanol-exposed pups. It has been observed that treatment with CA attenuates the altered cognitive function in ethanol-exposed pups. There was a significant decrease in the activity of acetylcholinesterase in the CA treated group compared to the negative control group. However, treatment with CA significantly ameliorates the increased oxidative stress and concentration of inflammatory mediators in the brain tissues of ethanol-exposed pups. Activity of caspase-3 enzyme was also found significantly decreased in the CA treated group compared to the negative control group. The present study concludes that CA attenuates the neuronal damage induced in alcohol exposed neonatal rat by decreasing the apoptosis of neuronal cells.


2016 ◽  
Vol 34 (3) ◽  
pp. 367-377 ◽  
Author(s):  
Jae-Young Han ◽  
Jung-Kook Kim ◽  
Jae-Hong Kim ◽  
Bong-Seok Oh ◽  
Wan-Ju Cho ◽  
...  

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