scholarly journals Ethyl-acetate fraction of Trichilia catigua protects against oxidative stress and neuroinflammation after cerebral ischemia/reperfusion

2018 ◽  
Vol 221 ◽  
pp. 109-118 ◽  
Author(s):  
Jacqueline Godinho ◽  
Anacharis Babeto de Sa-Nakanishi ◽  
Lucas Stafuza Moreira ◽  
Rúbia Maria Weffort de Oliveira ◽  
Claudia Hitomi Huzita ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Ethyl Acetate ◽  
Ischemia Reperfusion ◽  
Ethyl Acetate Fraction ◽  
Cerebral Ischemia Reperfusion

Neuroprotection of chromobox 7 knockout in the mouse after cerebral ischemia-reperfusion injury via nuclear factor E2-related factor 2/hemeoxygenase-1 signaling pathway

2021 ◽  
pp. 096032712110361
Author(s):  
Hai-Tao Zhang ◽  
Xi-Zeng Wang ◽  
Qing-Mei Zhang ◽  
Han Zhao
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Infarct Size ◽  
Water Content ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion ◽  
Related Factor ◽  
Nuclear Factor ◽  
Cerebral Ischemia Reperfusion ◽  
And Oxidative Stress

Objective To explore the mechanism of chromobox 7 (CBX7)-mediated nuclear factor E2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway in the cerebral ischemia/reperfusion (I/R) injury. Methods The experimental wild-type (WT) and CBX7-/- mice were used to establish cerebral I/R models using the middle cerebral artery occlusion (MCAO) surgery to determine CBX7 levels at different time points after MCAO injury. For all mice, neurological behavior, infarct size, water content, and oxidative stress–related indicators were determined, and transferase (TdT)-mediated dUTP-biotin nick-end labeling (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL)) staining method was employed to observe cell apoptosis, while Western blot to measure the expression of CBX7 and Nrf/HO-1 pathway-related proteins. Results At 6 h, 12 h, 24 h, 3 days, and 7 days after mice with MCAO, CBX7 expression was gradually up-regulated and the peak level was reached at 24 h. Mice in the WT + MCAO group had increased infarct size, with significant increases in the modified neurological severity scores and water content in the brain, as well as the quantity of TUNEL-positive cells. For the oxidative stress-indicators, an increase was seen in the content of MDA (malondial dehyde), but the activity of SOD (superoxide dismutase) and content of GSH-PX (glutathione peroxidase) and CAT (catalase) were decreased; meanwhile, the protein expression of CBX7, HO-1, and nuclear Nrf2 was up-regulated, while the cytoplasmic Nrf2 was down-regulated. Moreover, CBX7 knockout attenuated I/R injury in mice. Conclusion Knockout of CBX7 may protect mice from cerebral I/R injury by reducing cell apoptosis and oxidative stress, possibly via activating the Nrf2/HO-1 pathway.

Ethyl-acetate fraction of Trichilia catigua restores long-term retrograde memory and reduces oxidative stress and inflammation after global cerebral ischemia in rats

2018 ◽  
Vol 337 ◽  
pp. 173-182 ◽  
Author(s):  
Jacqueline Godinho ◽  
Rúbia Maria Weffort de Oliveira ◽  
Anacharis Babeto de Sa-Nakanishi ◽  
Cristiano Correia Bacarin ◽  
Claudia Hitomi Huzita ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Ethyl Acetate ◽  
Ethyl Acetate Fraction ◽  
Global Cerebral Ischemia ◽  
Retrograde Memory

Transcriptional Regulation of Antioxidant Enzymes Activity and Modulation of Oxidative Stress by Melatonin in Rats Under Cerebral Ischemia / Reperfusion Conditions

Neuroscience ◽  
2019 ◽  
Vol 406 ◽  
pp. 653-666 ◽  
Author(s):  
Evgenii D. Kryl'skii ◽  
Tatyana N. Popova ◽  
Olga A. Safonova ◽  
Anna O. Stolyarova ◽  
Grigorii A. Razuvaev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcriptional Regulation ◽  
Antioxidant Enzymes ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Enzymes Activity ◽  
Cerebral Ischemia Reperfusion

Effects of Normobaric Hyperoxia in a Rat Model of Focal Cerebral Ischemia—Reperfusion

2002 ◽  
Vol 22 (7) ◽  
pp. 861-868 ◽  
Author(s):  
Aneesh B. Singhal ◽  
Xiaoying Wang ◽  
Toshihisa Sumii ◽  
Tatsuro Mori ◽  
Eng H. Lo
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Protein Carbonyl ◽  
Blue Dye ◽  
Heme Oxygenase 1 ◽  
Normobaric Hyperoxia ◽  
Cerebral Ischemia Reperfusion ◽  
Carbonyl Formation

Recent studies suggest that normobaric hyperoxia can be beneficial, if administered during transient stroke. However, increased oxygenation theoretically may increase oxygen free-radical injury, particularly during reperfusion. In the present study, the authors assessed the benefit and risks of hyperoxia during focal cerebral ischemia and reperfusion. Rats were subjected to hyperoxia (Fio2 100%) or normoxia (Fio2 30%) during 2-hour filament occlusion and 1-hour reperfusion of the middle cerebral artery. At 24 hours, the hyperoxia group showed 70% (total) and 92% (cortical) reduction in infarct volumes as compared to the normoxia group. Levels of oxidative stress were evaluated using three indirect methods. First, since oxygen free radicals increase blood—brain barrier (BBB) damage, Evan's blue dye extravasation was quantified to assess BBB damage. Second, the expression of heme oxygenase-1 (HO-1), a heat shock protein inducible by oxidative stress, was assessed using Western blot techniques. Third, an immunoblot technique (“OxyBlot”) was used to assess levels of protein carbonyl formation as a marker of oxidative stress—induced protein denaturation. At 24 hours, Evan's blue dye extravasation per average lesion volume was similar between groups. There were no significant differences in HO-1 induction and protein carbonyl formation between groups, in the ipsilateral or contralateral hemispheres, at 6 hours and at 24 hours. These results indicate that hyperoxia treatment during focal cerebral ischemia—reperfusion is neuroprotective, and does not increase oxidative stress.

Nomilin protects against cerebral ischemia–reperfusion induced neurological deficits and blood–brain barrier disruption via the Nrf2 pathway

2019 ◽  
Vol 10 (9) ◽  
pp. 5323-5332 ◽  
Author(s):  
Yu-Sheng Shi ◽  
Yan Zhang ◽  
Bin Liu ◽  
Chun-Bin Li ◽  
Jiao Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neurological Deficits ◽  
Nrf2 Pathway ◽  
Blood Brain Barrier Disruption ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Brain Barrier Disruption

Oxidative stress is considered to play an important role in the cerebral ischemia–reperfusion injury.

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