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 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.

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.

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 Chronic Cerebral Hypoperfusion Induces Vascular Plasticity and Hemodynamics but Also Neuronal Degeneration and Cognitive Impairment

2015 ◽  
Vol 35 (8) ◽  
pp. 1249-1259 ◽  
Author(s):  
Zhen Jing ◽  
Changzheng Shi ◽  
Lihui Zhu ◽  
Yonghui Xiang ◽  
Peihao Chen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Neuronal Degeneration ◽  
Neuronal Loss ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Common Carotid Artery Occlusion

Chronic cerebral hypoperfusion (CCH) induces cognitive impairment, but the compensative mechanism of cerebral blood flow (CBF) is not fully understood. The present study mainly investigated dynamic changes in CBF, angiogenesis, and cellular pathology in the cortex, the striatum, and the cerebellum, and also studied cognitive impairment of rats induced by bilateral common carotid artery occlusion (BCCAO). Magnetic resonance imaging (MRI) techniques, immunochemistry, and Morris water maze were employed to the study. The CBF of the cortex, striatum, and cerebellum dramatically decreased after right common carotid artery occlusion (RCCAO), and remained lower level at 2 weeks after BCCAO. It returned to the sham level from 3 to 6 weeks companied by the dilation of vertebral arteries after BCCAO. The number of microvessels declined at 2, 3, and 4 weeks but increased at 6 weeks after BCCAO. Neuronal degeneration occurred in the cortex and striatum from 2 to 6 weeks, but the number of glial cells dramatically increased at 4 weeks after BCCAO. Cognitive impairment of ischemic rats was directly related to ischemic duration. Our results suggest that CCH induces a compensative mechanism attempting to maintain optimal CBF to the brain. However, this limited compensation cannot prevent neuronal loss and cognitive impairment after permanent ischemia.

scholarly journals Acupuncture Rescues Cognitive Impairment and Upregulates Dopamine-β-Hydroxylase Expression in Chronic Cerebral Hypoperfusion Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ling-Yong Xiao ◽  
Jing-Wen Yang ◽  
Xue-Rui Wang ◽  
Yang Ye ◽  
Na-Na Yang ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Vessel Occlusion ◽  
Memory Impairments ◽  
Beneficial Effects ◽  
Hippocampus Dependent Memory

Alteration of dopamine (DA) and noradrenaline (NA) contributes to cognitive function. Acupuncture has been shown to affect DA and NA in chronic cerebral hypoperfusion (CCH) rats. However, the effect of acupuncture on DA-β-hydroxylase (DBH), the biosynthetic enzyme of NA, remains unknown. In CCH rats we established chronic hypoperfusion by bilateral common carotid artery occlusion (two-vessel occlusion, 2VO) and treated them with acupuncture. Acupuncture displayed beneficial effects on hippocampus-dependent memory impairments, including nonspatial and spatial memory. That is also reflected in hippocampus long-term-potentiation (LTP). Moreover, DBH expression in the hippocampus and DBH activity in cerebrospinal fluid were upregulated after acupuncture treatment. In conclusion, these in vivo findings suggest that acupuncture exerts a therapeutic effect on hippocampus-dependent memory and hippocampus LTP in CCH rats, which may be partially related to the modulation of DBH in the hippocampus.

scholarly journals Impaired Cognitive Flexibility Induced by Chronic Cerebral Hypoperfusion in the 5XFAD Transgenic Mouse Model of Mixed Dementia

2021 ◽  
Author(s):  
Min-Soo Kim ◽  
Jihye Bang ◽  
Bu-Yeo Kim ◽  
Won Kyung Jeon
Keyword(s):  
Mouse Model ◽  
Cognitive Flexibility ◽  
Cognitive Strategies ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Plaque Burden ◽  
Cerebrovascular Lesions ◽  
Aβ Clearance

Abstract Cerebrovascular lesions are widely prevalent in patients with Alzheimer’s disease (AD), but their relationship to the pathophysiology of AD remains poorly understood. An improved understanding of the interaction of cerebrovascular damage with AD is crucial for the development of therapeutic approaches. Herein, we investigated the effects of chronic cerebral hypoperfusion (CCH) in a 5XFAD transgenic (Tg) mouse model of AD. We established CCH conditions in both Tg and non-Tg mice by inducing unilateral common carotid artery occlusion (UCCAO). Cognitive performance in mice was evaluated, and their brain tissue was examined for amyloid-beta (Aβ) pathology to elucidate possible mechanisms. We found that UCCAO-operated Tg mice showed impaired cognitive flexibility in the reversal phase of the hidden-platform water maze task compared to sham-operated Tg mice. Interestingly, UCCAO-operated Tg mice used fewer spatial cognitive strategies than sham-operated Tg mice during reversal learning. These cognitive deficits were accompanied by increased Aβ plaque burden and Aβ42 levels in the hippocampus and prefrontal cortex, 2 regions that play essential roles in the regulation of cognitive flexibility. Furthermore, changes in cognitive flexibility are strongly correlated with the expression levels of enzymes related to Aβ clearance, such as neprilysin and insulin-degrading enzymes. These findings suggest that, in 5XFAD mice, impaired cognitive flexibility is related to CCH, and that Aβ clearance might be involved in this process.

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