Protective effects of banana pectin against aluminum-induced cognitive impairment and aluminum accumulation in mice

2018 ◽  
Vol 41 (3) ◽  
pp. 294-301 ◽  
Author(s):  
Xiangquan Zeng ◽  
Xiaomei Wang ◽  
Handong Zhao ◽  
Yu Xi ◽  
Jiankang Cao ◽  
...  
2020 ◽  
Author(s):  
Shao-Peng Lin ◽  
Jue-Xian Wei ◽  
Shan Ye ◽  
Jiasong Hu ◽  
Jingyi Bu ◽  
...  

Abstract Background and purpose: Artemisinin has been in use as an anti-malarial drug for almost half a century in the world. There is growing evidence that artemisinin also possesses potent anti-inflammatory and immunoregulatory properties. However, the efficacy of artemisinin treatment in neurocognitive deficits associated with sepsis remains unknown. Here, we evaluate the possible protective effects and explore the underlying mechanism of artemisinin on cognitive impairment resulting from sepsis.Methods: Male C57BL/6 mice were pretreated with either vehicle or artemisinin, and then injected with LPS to establish an animal model of sepsis. The cognitive function was then assessed using the Morris water maze. Neuronal damage and neuroinflammation in the hippocampus were evaluated by immunohistochemical and ELISA analysis. Additionally, the protective mechanism of artemisinin was determined in vitro.Results: The results showed that artemisinin preconditioning attenuated LPS-induced cognitive impairment, neural damage, and microglial activation in the mouse brain. The in vitro experiment revealed that artemisinin could reduce the production of pro-inflammatory cytokines and suppress the microglial migration in the BV2 microglia cells. Meanwhile, western blot demonstrated that artemisinin suppressed nuclear translocation of nuclear factor kappa-B and the expression of pro-inflammatory cytokines (i.e. tumor necrosis factor alpha, interleukin-6) by activating adenosine monophosphate-activated protein kinaseα1 (AMPKα1) pathway. Furthermore, knock-down of AMPKα1 markedly abolished the anti-inflammatory effects of artemisinin.Conclusion: Artemisinin is a potential therapeutic agent for sepsis-associated neuroinflammation and cognitive impairment, and its effect was probably mediated by the activation of AMPKα1 signalling pathway in microglia.


2020 ◽  
Vol 73 ◽  
pp. 104089
Author(s):  
Xiaoqin He ◽  
Yong Tian ◽  
Lin Lei ◽  
Qi Zhi ◽  
Jichun Zhao ◽  
...  

2017 ◽  
Vol 36 (12) ◽  
pp. 1295-1302 ◽  
Author(s):  
L Liang ◽  
Z Ma ◽  
M Dong ◽  
J Ma ◽  
A Jiang ◽  
...  

Postoperative cognitive dysfunction, which is associated with a wide range of cognitive functions including working memory, long-term memory, information processing, attention, and cognitive flexibility, is a major clinical issue in geriatric surgical patients. The aim of the current study was to determine the protective role and possible mechanisms of salidroside against isoflurane-induced cognitive impairment. Sprague Dawley rats were randomly assigned to five groups and were treated with or without salidroside before isoflurane exposure. Open-field and fear conditioning tests were conducted to evaluate the cognitive function of the rats. Moreover, the hippocampus tissues were obtained for biochemical analysis. The results showed that the isoflurane anesthesia decreased the freezing time to context significantly at 48 h after the isoflurane exposure in the fear conditioning test. Salidroside could ameliorate isoflurane-induced cognitive dysfunction. Further analysis demonstrated salidroside markedly suppressed the release of tumor necrosis factor-α and interleukin-1β. Moreover, salidroside reversed the decreased activity of choline acetyltransferase, superoxide dismutase, glutathione peroxidase, and content of acetylcholine, as well as the increased activity of acetylcholine esterase and content of malondialdehyde in hippocampal tissue of isoflurane-exposed rats. According to the results, we concluded that that salidroside has a protective effect against isoflurane-induced cognitive dysfunction by inhibiting excessive inflammatory responses, decreasing oxidative stress, and regulating the cholinergic system.


2008 ◽  
Vol 193 (5) ◽  
pp. 351-353 ◽  
Author(s):  
Susham Gupta ◽  
James Warner

SummaryEvidence suggests a J-shaped relationship between alcohol consumption and cognitive impairment and other health indicators, with low levels of consumption having better outcomes than abstention or moderate to heavy drinking. Most research to date has focused on the protective effects of drinking small amounts of alcohol. As alcohol consumption is escalating rapidly in many countries, the current cohort of young and middle-aged people may face an upsurge of alcohol-related dementia. The dangers of heavy drinking and its effect on cognition require further attention.


2018 ◽  
Author(s):  
Jeremy A. Elman ◽  
Matthew S. Panizzon ◽  
Mark W. Logue ◽  
Nathan A. Gillespie ◽  
Michael C. Neale ◽  
...  

ABSTRACTBACKGROUNDAlzheimer’s disease (AD) is under considerable genetic influence. However, known susceptibility loci only explain a modest proportion of variance in disease outcomes. This small proportion could occur if the etiology of AD is heterogeneous. We previously found that an AD polygenic risk score (PRS) was significantly associated with mild cognitive impairment (MCI), an early stage of AD. Poor cardiovascular health is also associated with increased risk for AD and has been found to interact with AD pathology. Conditions such as coronary artery disease (CAD) are also heritable, and may contribute to heterogeneity if there are interactions of genetic risk for these conditions as there is phenotypically. However, case-control designs based on prevalent cases of a disease with relatively high case-fatality rate such as CAD may be biased toward individuals who have long post-event survival times and may therefore also identify loci with protective effects.METHODSWe compared interactions between an AD-PRS and two CAD-PRSs, one based on a GWAS of incident cases and one on prevalent cases, on MCI status in 1,209 individuals.RESULTSAs expected, the incidence-based CAD-PRS interacts with the AD-PRS to further increase MCI risk. Conversely, higher prevalence-based CAD-PRSs reduced the effect of AD genetic risk on MCI status.CONCLUSIONSThese results demonstrate: i) the utility of including multiple PRSs and their interaction effects; ii) how genetic risk for one disease may modify the impact of genetic risk for another; and iii) the importance of considering ascertainment procedures of GWAS being used for genetic risk prediction.


Molecules ◽  
2021 ◽  
Vol 26 (23) ◽  
pp. 7085
Author(s):  
Luminita Capatina ◽  
Edoardo Marco Napoli ◽  
Giuseppe Ruberto ◽  
Lucian Hritcu

Origanum vulgare ssp. hirtum has been used as medicinal herbs promoting antioxidant, anti-inflammatory, antimicrobial, and neuroprotective activities. We investigated the protective effects and the mechanism of O. vulgare ssp. hirtum essential oil (OEO) on cognitive impairment and brain oxidative stress in a scopolamine (Sco)-induced zebrafish (Danio rerio) model of cognitive impairment. Our results show that exposure to Sco (100 µM) leads to anxiety, spatial memory, and response to novelty dysfunctions, whereas the administration of OEO (25, 150, and 300 µL/L, once daily for 13 days) reduced anxiety-like behavior and improved cognitive ability, which was confirmed by behavioral tests, such as the novel tank-diving test (NTT), Y-maze test, and novel object recognition test (NOR) in zebrafish. Additionally, Sco-induced brain oxidative stress and increasing of acetylcholinesterase (AChE) activity were attenuated by the administration of OEO. The gas chromatography–mass spectrometry (GC-MS) analyses were used to elucidate the OEO composition, comprising thymol (38.82%), p-cymene (20.28%), and γ-terpinene (19.58%) as the main identified components. These findings suggest the ability of OEO to revert the Sco-induced cognitive deficits by restoring the cholinergic system activity and brain antioxidant status. Thus, OEO could be used as perspective sources of bioactive compounds, displaying valuable biological activities, with potential pharmaceutical applications.


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