scholarly journals Electroacupuncture Attenuates Cognitive Impairment in Rat Model of Chronic Cerebral Hypoperfusion via miR-137/NOX4 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Xiaochen Bi ◽  
Yanfei Feng ◽  
Zemin Wu ◽  
Jianqiao Fang
Keyword(s):  
Oxidative Stress ◽  
Neuronal Apoptosis ◽  
Molecular Mechanisms ◽  
Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Control Group ◽  
Spatial Learning And Memory ◽  
Protective Effects ◽  
And Oxidative Stress

Electroacupuncture has shown protective effects on cognitive decline. However, the underlying molecular mechanisms are not clear. The present study was conducted to determine whether the cognitive function was ameliorated in cerebral hypoperfusion rats following electroacupuncture and to investigate the role of miR-137/NOX4 axis. In this study, chronic cerebral hypoperfusion (CCH) model was established by bilateral common carotid artery occlusion. Electroacupuncture treatment attenuated brain injury in CCH model group via regulating miR-137/NOX4 axis. Furthermore, the data of neuronal apoptosis and oxidative stress were observed. Our findings indicated that (1) neuronal apoptosis and oxidative stress in CCH rats were significantly increased compared with control group; (2) the animal cognitive performance was evaluated using the Morris water maze (MWM). The results showed that electroacupuncture therapy ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; and (3) electroacupuncture therapy reduces neuronal apoptosis and oxidative stress by activating miR-137/NOX4 axis. These results suggest that electroacupuncture therapy for CCH may be mediated by miR-137/NOX4 axis. Electroacupuncture therapy may act as a potential therapeutic approach for chronic cerebral hypoperfusion.

Effect of endogenous sulfur dioxide on spatial learning and memory and hippocampal damages in the experimental model of chronic cerebral hypoperfusion

2020 ◽  
Vol 31 (3) ◽  
Author(s):  
Elaheh Ghasemi ◽  
Faezeh Afkhami Aghda ◽  
Mohammad Ebrahim Rezvani ◽  
Azadeh Shahrokhi Raeini ◽  
Zeynab Hafizibarjin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sulfur Dioxide ◽  
Tissue Damage ◽  
Neuronal Damage ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Vital Role ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Spatial Learning And Memory

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.

scholarly journals Environmental enrichment prevents behavioral deficits and oxidative stress caused by chronic cerebral hypoperfusion in the rat

Life Sciences ◽  
2012 ◽  
Vol 91 (1-2) ◽  
pp. 29-36 ◽  
Author(s):  
Fernanda Cechetti ◽  
Paulo Valdeci Worm ◽  
Gisele Lovatel ◽  
Felipe Moysés ◽  
Ionara Rodrigues Siqueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Environmental Enrichment ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Behavioral Deficits ◽  
And Oxidative Stress

Vitexin regulates EPAC and NLRP3 and ameliorates chronic cerebral hypoperfusion injury

2021 ◽  
Author(s):  
Qilong Zhang ◽  
Zhijia Fan ◽  
wei xue ◽  
Fanfan Sun ◽  
Huaqing Zhu ◽  
...  
Keyword(s):  
Neuronal Damage ◽  
Critical Factor ◽  
Underlying Mechanism ◽  
Cerebrovascular Diseases ◽  
Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Protective Effects ◽  
Ht22 Cells

Chronic cerebral hypoperfusion (CCH), as a critical factor of chronic cerebrovascular diseases, has greatly influenced the health of patients with vascular dementia (VD). The putative protective effects of vitexin on the CCH need further investigations. In the current study, the role of vitexin and its underlying mechanism were investigated with permanent bilateral common carotid artery occlusion (2VO) in rats as well as HT22 cells with OGD/R injury model. The results demonstrated that vitexin improved cognitive dysfunction as well as alleviated pathological neuronal damage in HE and TUNEL results. The decreased levels of Epac1, Epac2, Rap1 and p-ERK were reversed by vitexin in rats with CCH. Furthermore, this study indicated that vitexin alleviated CCH-induced inflammation injuries by reducing the expression of NLRP3, Caspase-1, IL-1β, IL-6, and cleaved Caspase-3. In vitro, vitexin increased the expression of Epac1 and Epac2, decreased the activation of the NLRP3-mediated inflammation, and improved cell viability. Taken together, our findings suggest that vitexin can reduce the degree of the progressing pathological damage in the cortex and hippocampus and inhibit further deterioration of cognitive function in rats with CCH. Epac and NLRP3 can be regulated by vitexin, which provides enlightenment for the protection of CCH injury.

scholarly journals Effects ofFructus mumeExtract on MAPK and NF-κB Signaling and the Resultant Improvement in the Cognitive Deficits Induced by Chronic Cerebral Hypoperfusion

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Won Kyung Jeon ◽  
Jinhua Ma ◽  
Bo-Ryoung Choi ◽  
Seol-Heui Han ◽  
Qinghao Jin ◽  
...  
Keyword(s):  
Microglial Activation ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Mitogen Activated Protein Kinase ◽  
Daily Administration ◽  
Cerebral Hypoperfusion ◽  
Memory Impairments ◽  
The Status

Fructus mume(F. mume) has been used as a medicinal food in Japan and has been reported to have anti-inflammatory effects in inflammatory bowel disease and macrophage-mediated inflammation. We investigated the effects ofF. mumeextracts on cognitive dysfunction in rats with chronic cerebral hypoperfusion and the molecular mechanisms underlying these effects. Chronic cerebral hypoperfusion was induced in male Wister rats by bilateral common artery occlusion (BCCAo). Daily administration ofF. mumeextracts was started on day 20 after post-BCCAo and continued for 40 days. The status of hippocampus-dependent memory was evaluated in control rats, rats with chronic cerebral hypoperfusion, and rats with chronic cerebral hypoperfusion that were administeredF. mume. The levels of microglial activation were measured in the hippocampus and the fimbria of hippocampus, and expression levels of hippocampal mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) were examined. Rats that received chronic cerebral hypoperfusion showed spatial memory impairments relative to the control rats; these impairments were reduced by daily administration ofF. mume. Administration ofF. mumemitigated the microglial activation and alterations of hippocampal MAPK and NF-κB signaling in the rats with chronic cerebral hypoperfusion. These results indicate thatF. mumemay possess therapeutic potential for the prevention of vascular dementia via inhibition of inflammatory processes.

Protective effects of Chrysin against memory impairment, cerebral hyperemia and oxidative stress after cerebral hypoperfusion and reperfusion in rats

2019 ◽  
Vol 35 (2) ◽  
pp. 401-412 ◽  
Author(s):  
Maryam Khombi Shooshtari ◽  
Alireza Sarkaki ◽  
Seyed Mohammad Taghi Mansouri ◽  
Mohammad Badavi ◽  
Layasadat Khorsandi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Memory Impairment ◽  
Cerebral Hypoperfusion ◽  
Protective Effects ◽  
And Oxidative Stress

scholarly journals Germacrone alleviates neurological deficits following traumatic brain injury by modulating neuroinflammation and oxidative stress

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sujing Zhuang ◽  
Baogui Liu ◽  
Shifeng Guo ◽  
Yanzhong Xue ◽  
Lin Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Neuronal Apoptosis ◽  
Spatial Learning And Memory ◽  
Dependent Manner ◽  
Dose Dependent ◽  
And Oxidative Stress

Abstract Background Germacrone (GM) is a terpenoid compound which is reported to have anti-inflammatory and anti-oxidative effects. However, its role in treating traumatic brain injury (TBI) remains largely unknown. Methods Male C57BL/6 mice were divided into the following groups: control group, TBI group [controlled cortical impact (CCI) model], CCI + 5 mg/kg GM group, CCI + 10 mg/kg GM group and CCI + 20 mg/kg GM group. GM was administered via intraperitoneal injection. The neurological functions (including motor coordination, spatial learning and memory abilities) and brain edema were measured. Nissl staining was used to detect the neuronal apoptosis. Colorimetric assays and enzyme linked immunosorbent assay (ELISA) kits were used to determine the expression levels of oxidative stress markers including myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD), as well as the expressions of inflammatory markers, including tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Additionally, protein levels of Nrf2 and p-p65 were detected by Western blot assay. Results GM significantly ameliorated motor dysfunction, spatial learning and memory deficits of the mice induced by TBI and it also reduced neuronal apoptosis and microglial activation in a dose-dependent manner. Besides, GM treatment reduced neuroinflammation and oxidative stress compared to those in the CCI group in a dose-dependent manner. Furthermore, GM up-regulated the expression of antioxidant protein Nrf2 and inhibited the expression of inflammatory response protein p-p65. Conclusions GM is a promising drug to improve the functional recovery after TBI via repressing neuroinflammation and oxidative stress.

scholarly journals Apocynin promotes neural function recovery and suppresses neuronal apoptosis by inhibiting Tlr4/NF-κB signaling pathway in a rat model of cerebral infarction

2018 ◽  
Vol 32 ◽  
pp. 205873841881770
Author(s):  
Lemen Pan ◽  
Shuxia Qian
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cerebral Infarction ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neuronal Apoptosis ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion ◽  
And Oxidative Stress

Occlusion of arteries in the brain is a common cause of cerebral infarction which induces inflammatory response and oxidative stress resulting in neuronal apoptosis and disruption of neurological function. The present study investigated the protective roles of an nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin, against cerebral infarction. Rat went through a surgery of middle cerebral artery occlusion and a subset of rats was treated with apocynin by intraperitoneal injection. The volume of cerebral infarction and water content were measured. Neuronal apoptosis, inflammatory response, and oxidative stress were assessed following middle cerebral artery occlusion and apocynin treatment. We found that apocynin significantly improved neurological function, increased forelimb placement test scores, and suppressed balance beam walk latency in rats with cerebral infarction. Histological and biochemistry analysis revealed that apocynin lead to a significant reduction in the volume of cerebral infarction as well as cerebral water content, suppressed neuronal apoptosis, oxidative stress, and inflammatory response induced by middle cerebral artery occlusion. Finally, we found that apocynin suppressed Tlr4/nuclear factor-k-gene binding signaling pathway that was upregulated in rats with cerebral infarction. Our results indicate that apocynin may represent a potent therapeutic strategy in alleviating neurological dysfunctions in patients with cerebral infarction.

The effect of epigallocatechin-3-gallate on morphine-induced memory impairments in rat: EGCG effects on morphine neurotoxicity

2020 ◽  
Vol 39 (7) ◽  
pp. 994-1002 ◽  
Author(s):  
S Saffar ◽  
I Fatemi ◽  
M Rahmani ◽  
J Hassanshahi ◽  
A Sahamsizadeh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Morris Water Maze Test ◽  
Spatial Learning And Memory ◽  
Egcg Treatment ◽  
Memory Impairments ◽  
Protein Levels ◽  
Male Wistar Rats ◽  
Tea Extract ◽  
And Oxidative Stress

Aim of study: This investigation evaluated the capacity of epigallocatechin-3-gallate (EGCG) as the main polyphenolic compound in the green tea extract against memory impairment and neurotoxicity in morphine-treated rats. Methods: To measure the EGCG effect (5 and 50 mg/kg, i.p., co-treated with morphine) on spatial learning and memory of morphine-administrated male Wistar rats (45 mg/kg, s.c., 4 weeks), the Morris water maze test was used. Some apoptotic protein levels (Bax, Bcl-2, and cleaved caspase 3) were evaluated in the hippocampus tissue by the Western blot test. Also, oxidative stress status (malondialdehyde level, glutathione peroxidase, and superoxide dismutase activity) was measured in hippocampus tissue. Results: The data presented that EGCG treatment (50 mg/kg) inhibited the morphine-induced memory deficits in rats. Also, EGCG administration reduced the apoptosis and oxidative stress in the hippocampus of morphine-treated rats. Conclusions: Our data indicate that EGCG can improve memory in morphine-treated rats. Molecular mechanisms underlying the detected effects could be related to the prevention of apoptosis and oxidative stress in the hippocampus of morphine-treated rats.

scholarly journals NXP031 Improves Cognitive Impairment in a Chronic Cerebral Hypoperfusion-Induced Vascular Dementia Rat Model through Nrf2 Signaling

2021 ◽  
Vol 22 (12) ◽  
pp. 6285
Author(s):  
Jae-Min Lee ◽  
Joo-Hee Lee ◽  
Min-Kyung Song ◽  
Youn-Jung Kim
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Vitamin C ◽  
Vascular Dementia ◽  
Brain Regions ◽  
Artery Occlusion ◽  
Vital Role ◽  
Chronic Cerebral Hypoperfusion ◽  
Dna Aptamer ◽  
Cerebral Hypoperfusion

Vascular dementia (VaD) is a progressive cognitive impairment caused by a reduced blood supply to the brain. Chronic cerebral hypoperfusion (CCH) is one cause of VaD; it induces oxidative stress, neuroinflammation, and blood-brain barrier (BBB) disruption, damaging several brain regions. Vitamin C plays a vital role in preventing oxidative stress-related diseases induced by reactive oxygen species, but it is easily oxidized and loses its antioxidant activity. To overcome this weakness, we have developed a vitamin C/DNA aptamer complex (NXP031) that increases vitamin C’s antioxidant efficacy. Aptamers are short single-stranded nucleic acid polymers (DNA or RNA) that can interact with their corresponding target with high affinity. We established an animal model of VaD by permanent bilateral common carotid artery occlusion (BCCAO) in 12 week old Wistar rats. Twelve weeks after BCCAO, we injected NXP031 into the rats intraperitoneally for two weeks at moderate (200 mg/4 mg/kg) and high concentrations (200 mg/20 mg/kg). NXP031 administration alleviates cognitive impairment, microglial activity, and oxidative stress after CCH. NXP031 increased the expression of basal lamina (laminin), endothelial cell (RECA-1, PECAM-1), and pericyte (PDGFRβ); these markers maintain the BBB integrity. We found that NXP031 administration activated the Nrf2-ARE pathway and increased the expression of SOD-1 and GSTO1/2. These results suggest that this new aptamer complex, NXP031, could be a therapeutic intervention in CCH-induced VaD.

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