Cordycepin Ameliorates Intracerebral Hemorrhage Induced Neurological and Cognitive Impairments Through Reducing Anti-Oxidative Stress in a Mouse Model

2022 ◽  
Vol 31 (1) ◽  
pp. 106199
Author(s):  
Qingbao Yan ◽  
Haidong Zhang ◽  
Kai Hui ◽  
Qi Shao
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Cognitive Impairments

scholarly journals 17β-Estradiol Attenuates Intracerebral Hemorrhage-Induced Blood–Brain Barrier Injury and Oxidative Stress Through SRC3-Mediated PI3K/Akt Signaling Pathway in a Mouse Model

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142110384
Author(s):  
Han Xiao ◽  
Jianyang Liu ◽  
Jialin He ◽  
Ziwei Lan ◽  
Mingyang Deng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Signaling Pathway ◽  
Brain Edema ◽  
Akt Signaling ◽  
Neurological Deficits ◽  
Akt Signaling Pathway ◽  
And Oxidative Stress

Estrogen is neuroprotective in brain injury models, and steroid receptor cofactor 3 (SRC3) mediates estrogen signaling. We aimed to investigate whether and how SRC3 is involved in the neuroprotective effects of 17ß-estradiol (E2) in a mouse model of intracerebral hemorrhage (ICH). Ovariectomized female mice were treated with E2 after autologous blood injection-induced ICH. Brain damage was assessed by neurological deficit score, brain water content, and oxidative stress levels. Blood–brain barrier (BBB) integrity was evaluated by Evan's blue extravasation and claudin-5, ZO-1, and occludin levels. SRC3 expression and PI3K/Akt signaling pathway were examined in ICH mice treated with E2. The effect of SRC3 on E2-mediated neuroprotection was determined by examining neurological outcomes in SRC3-deficient mice undergone ICH and E2 treatment. We found that E2 alleviated ICH-induced brain edema and neurological deficits, protected BBB integrity, and suppressed oxidative stress. E2 enhanced SRC3 expression and PI3K-/Akt signaling pathway. SRC3 deficiency abolished the protective effects of E2 on ICH-induced neurological deficits, brain edema, and BBB integrity. Our results suggest that E2 suppresses ICH-induced brain injury and SRC3 plays a critical role in E2-mediated neuroprotection.

Effects of Donepezil on Oxidative Stress and Cognitive Impairments in a Mouse Model of Familial Hypercholesterolemia

2015 ◽  
Vol 87 ◽  
pp. S31
Author(s):  
Jade de Oliveira ◽  
Jadna Bogado Lopes ◽  
Daiane Engel ◽  
Gabriela Cristina de Paula ◽  
Eduardo Luiz Gasnhar Moreira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Familial Hypercholesterolemia ◽  
Cognitive Impairments

SRC-3 Deficiency Exacerbates Neurological Deficits in a Mouse Model of Intracerebral Hemorrhage: Role of Oxidative Stress

2021 ◽  
Author(s):  
Mingyang Deng ◽  
Jianyang Liu ◽  
Jialin He ◽  
Ziwei Lan ◽  
Zhiping Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Neurological Deficits

Neuroprotective functions of calycosin against intracerebral hemorrhage-induced oxidative stress and neuroinflammation

2020 ◽  
Author(s):  
Cheng Chen ◽  
Jing Cui ◽  
Xiaoqi Ji ◽  
Li Yao
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Water Content ◽  
Inhibitory Effects ◽  
Oxidative Damages ◽  
Pathway Activation ◽  
Severity Scores ◽  
Oxidative Pathway ◽  
The Brain

Aim: To investigate whether calycosin affects the brain damages induced by intracerebral hemorrhage (ICH). Methods: ICH mouse model was established by injection of collagenase type VII. Results: 50 mg/kg calycosin showed significant inhibitory effects on ICH-induced brain impairment evaluated by modified neurologic severity scores and water content. In addition, the lesion volumes, blood accumulation and hemispheric enlargement were all dramatically reduced by calycosin treatment compared with those of vehicles. It was observed that calycosin repressed oxidative stress by enhancing Nrf2 anti-oxidative pathway and suppressed inflammation by blocking NACHT, NALP3 inflammasome and NF-κB pathway activation. Conclusion: Calycosin could protect the brain against the damages induced by ICH via inhibiting oxidative damages and inflammation.

scholarly journals Alleviation of Memory Deficit by Bergenin via the Regulation of Reelin and Nrf-2/NF-κB Pathway in Transgenic Mouse Model

2021 ◽  
Vol 22 (12) ◽  
pp. 6603
Author(s):  
Bushra Shal ◽  
Adnan Khan ◽  
Ashraf Ullah Khan ◽  
Rahim Ullah ◽  
Gowhar Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Neuroprotective Effect ◽  
Annexin V ◽  
Memory Deficit ◽  
Y Maze ◽  
Spatial Memory Deficit ◽  
Aβ Aggregation ◽  
Ft Ir ◽  
Reelin Signaling

The present study aims to determine the neuroprotective effect of Bergenin against spatial memory deficit associated with neurodegeneration. Preliminarily, the protective effect of Bergenin was observed against H2O2-induced oxidative stress in HT-22 and PC-12 cells. Further studies were performed in 5xFAD Tg mouse model by administering Bergenin (1, 30 and 60 mg/kg; orally), whereas Bergenin (60 mg/kg) significantly attenuated the memory deficit observed in the Y-maze and Morris water maze (MWM) test. Fourier transform-infrared (FT-IR) spectroscopy displayed restoration of lipids, proteins and their derivatives compared to the 5xFAD Tg mice group. The differential scanning calorimeter (DSC) suggested an absence of amyloid beta (Aβ) aggregation in Bergenin-treated mice. The immunohistochemistry (IHC) analysis suggested the neuroprotective effect of Bergenin by increasing Reelin signaling (Reelin/Dab-1) and attenuated Aβ (1–42) aggregation in hippocampal regions of mouse brains. Furthermore, IHC and western blot results suggested antioxidant (Keap-1/Nrf-2/HO-1), anti-inflammatory (TLR-4/NF-kB) and anti-apoptotic (Bcl-2/Bax/Caspase-3) effect of Bergenin. Moreover, a decrease in Annexin V/PI-stained hippocampal cells suggested its effect against neurodegeneration. The histopathological changes were reversed significantly by Bergenin. In addition, a remarkable increase in antioxidant level with suppression of pro-inflammatory cytokines, oxidative stress and nitric oxide production were observed in specific regions of the mouse brains.

scholarly journals Oxidative Stress and Mitochondrial Damage in Dry Age-Related Macular Degeneration Like NFE2L2/PGC-1α -/- Mouse Model Evoke Complement Component C5a Independent of C3

Biology ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 622
Author(s):  
Iswariyaraja Sridevi Gurubaran ◽  
Hanna Heloterä ◽  
Stephen Marry ◽  
Ali Koskela ◽  
Juha M. T. Hyttinen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Macular Degeneration ◽  
Complement Component ◽  
Factor H ◽  
Age Related Macular Degeneration ◽  
Related Factor ◽  
Complement Factor ◽  
Age Related ◽  
Dry Amd

Aging-associated chronic oxidative stress and inflammation are known to be involved in various diseases, e.g., age-related macular degeneration (AMD). Previously, we reported the presence of dry AMD-like signs, such as elevated oxidative stress, dysfunctional mitophagy and the accumulation of detrimental oxidized materials in the retinal pigment epithelial (RPE) cells of nuclear factor erythroid 2-related factor 2, and a peroxisome proliferator-activated receptor gamma coactivator 1-alpha (NFE2L2/PGC1α) double knockout (dKO) mouse model. Here, we investigated the dynamics of inflammatory markers in one-year-old NFE2L2/PGC1α dKO mice. Immunohistochemical analysis revealed an increase in levels of Toll-like receptors 3 and 9, while those of NOD-like receptor 3 were decreased in NFE2L2/PGC1α dKO retinal specimens as compared to wild type animals. Further analysis showed a trend towards an increase in complement component C5a independent of component C3, observed to be tightly regulated by complement factor H. Interestingly, we found that thrombin, a serine protease enzyme, was involved in enhancing the terminal pathway producing C5a, independent of C3. We also detected an increase in primary acute phase C-reactive protein and receptor for advanced glycation end products in NFE2L2/PGC1α dKO retina. Our main data show C5 and thrombin upregulation together with decreased C3 levels in this dry AMD-like model. In general, the retina strives to mount an orchestrated inflammatory response while attempting to maintain tissue homeostasis and resolve inflammation.

Aberrant adenosine A2A receptor signaling contributes to neurodegeneration and cognitive impairments in a mouse model of synucleinopathy

2016 ◽  
Vol 283 ◽  
pp. 213-223 ◽  
Author(s):  
Qidi Hu ◽  
Xiangpeng Ren ◽  
Ya Liu ◽  
Zhihui Li ◽  
Liping Zhang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Cognitive Impairments ◽  
Adenosine A2a Receptor ◽  
Receptor Signaling ◽  
A2a Receptor ◽  
Adenosine A2a

scholarly journals Cancer cachexia in a mouse model of oxidative stress

2020 ◽  
Vol 11 (6) ◽  
pp. 1688-1704 ◽  
Author(s):  
Jacob L. Brown ◽  
Marcus M. Lawrence ◽  
Bumsoo Ahn ◽  
Parker Kneis ◽  
Katarzyna M. Piekarz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Cancer Cachexia
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