scholarly journals Effects of Pueraria candollei var mirifica (Airy Shaw and Suvat.) Niyomdham on Ovariectomy-Induced Cognitive Impairment and Oxidative Stress in the Mouse Brain

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3442
Author(s):  
Yaowared Chulikhit ◽  
Wichitsak Sukhano ◽  
Supawadee Daodee ◽  
Waraporn Putalun ◽  
Rakvajee Wongpradit ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Morris Water Maze Test ◽  
Object Recognition Test ◽  
Pueraria Mirifica ◽  
Beneficial Effects ◽  
Maze Test ◽  
Y Maze ◽  
Tnf Α ◽  
17Β Estradiol

The effects of the phytoestrogen-enriched plant Pueraria mirifica (PM) extract on ovari-ectomy (OVX)-induced cognitive impairment and hippocampal oxidative stress in mice were investigated. Daily treatment with PM and 17β-estradiol (E2) significantly elevated cognitive behavior as evaluated by using the Y maze test, the novel object recognition test (NORT), and the Morris water maze test (MWM), attenuated atrophic changes in the uterus and decreased serum 17β-estradiol levels. The treatments significantly ameliorated ovariectomy-induced oxidative stress in the hippocampus and serum by a decrease in malondialdehyde (MDA), an enhancement of superoxide dismutase, and catalase activity, including significantly down-regulated expression of IL-1β, IL-6 and TNF-α proinflammatory cytokines, while up-regulating expression of PI3K. The present results suggest that PM extract suppresses oxidative brain damage and dysfunctions in the hippocampal antioxidant system, including the neuroinflammatory system in OVX animals, thereby preventing OVX-induced cognitive impairment. The present results indicate that PM exerts beneficial effects on cognitive deficits for which menopause/ovariectomy have been implicated as risk factors.

scholarly journals Cirsium japonicum var. Maackii Improves Cognitive Impairment under Amyloid Beta25-35-Induced Alzheimer’s Disease Model

2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Qi Qi Pang ◽  
Ji-Hyun Kim ◽  
Ji Myung Choi ◽  
Jia-Le Song ◽  
Sanghyun Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Object Recognition ◽  
Ethyl Acetate Fraction ◽  
Morris Water Maze Test ◽  
Dependent Manner ◽  
Object Recognition Test ◽  
Cirsium Japonicum

Abnormal production and degradation of amyloid beta (Aβ) in the brain lead to oxidative stress and cognitive impairment in Alzheimer’s disease (AD). Cirsium japonicum var. maackii (CJM) is widely used as an herbal medicine and has antibacterial and anti-inflammatory properties. This study focused on the protective effect of the ethyl acetate fraction from CJM (ECJM) on Aβ25-35-induced control mice. In the T-maze and novel object recognition test, ECJM provided higher spatial memory and object recognition compared to Aβ25-35 treatment alone. In the Morris water maze test, ECJM-administered mice showed greater learning and memory abilities than Aβ25-35-induced control mice. Additionally, ECJM-administered mice experienced inhibited lipid peroxidation and nitric oxide production in a dose-dependent manner. The present study indicates that ECJM improves cognitive impairment by inhibiting oxidative stress in Aβ25-35-induced mice. Therefore, CJM may be useful for the treatment of AD and may be a potential material for functional foods.

scholarly journals The Synergistic Beneficial Effects of Ginkgo Flavonoid andCoriolus versicolorPolysaccharide for Memory Improvements in a Mouse Model of Dementia

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Xianying Fang ◽  
Yan Jiang ◽  
Hui Ji ◽  
Linguo Zhao ◽  
Wei Xiao ◽  
...  
Keyword(s):  
Mouse Model ◽  
Coriolus Versicolor ◽  
Morris Water Maze Test ◽  
Beneficial Effects ◽  
Medicinal Fungus ◽  
Traditional Health ◽  
Maze Test ◽  
Model Of Alzheimer’S Disease ◽  
Y Maze ◽  
The Brain

This study reports the combination of Ginkgo flavonoid (GF) andCoriolus versicolorpolysaccharide (CVP) in the prevention and treatment of a mouse model of Alzheimer’s disease (AD). GF is a traditional health product, and CVP is the main active ingredient of the medicinal fungusCoriolus versicolor. The Morris water maze test, the Y maze, and the step-through test showed that the combinational use of CVP and GF synergistically improved memory in a mouse model of AD. Based on H&E staining analysis, the combination of CVP and GF decreased the severity of the pathological findings in the brain. Given that the expression of IL-1β, IL-6, and TNF-αwas downregulated, the inflammation response in AD mice was considered to be inhibited. The downregulation of GFAP further demonstrated that inflammation was reduced in the brain of AD mice following treatment. Moreover, the expression levels of superoxide dismutase (SOD) and catalase (CAT) were elevated in the brains of treated mice, indicating that oxidation levels were reduced upon the combination treatment. Our results provide new insights into the efficient utilization of traditional medicine for preventing dementia.

scholarly journals Selenomethionine Ameliorates Cognitive Impairment, Decreases Hippocampal Oxidative Stress and Attenuates Dysbiosis in D-Galactose-Treated Mice

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 111
Author(s):  
Ying Gao ◽  
Yongquan Xu ◽  
Junfeng Yin
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Morris Water Maze Test ◽  
Taxonomic Structure ◽  
Avoidance Task ◽  
Older Individuals ◽  
Object Recognition Test ◽  
Age Related ◽  
Structure Correlations ◽  
Α Diversity

The prevalence of age-related cognitive impairment is increasing as the proportion of older individuals in the population grows. It is therefore necessary and urgent to find agents to prevent or ameliorate age-related cognitive impairment. Selenomethionine (SeMet) is a natural amino acid occurring in yeast and Brazil nuts. It mitigates cognitive impairment in an Alzheimer’s disease mouse model, however, whether it works on age-related cognitive impairment remains unknown. In this study, SeMet significantly improved the performance of D-galactose-treated mice in the novel object recognition test, passive avoidance task and Morris water maze test. SeMet reversed D-galactose-induced reduction of hippocampal acetylcholine levels, suppression of choline acetyltransferase activity and activation of acetyl cholinesterase. It decreased D-galactose-induced oxidative stress and increased the selenoprotein P levels in the hippocampus. Besides, it attenuated D-galactose-induced dysbiosis by increasing the α-diversity and modulating the taxonomic structure. Correlations between certain taxa and physiological parameters were observed. Our results provide evidence of the effectiveness of SeMet on ameliorating D-galactose-induced cognitive impairment and suggest SeMet has potential to be used in the prevention or adjuvant treatment of age-related cognitive impairment.

scholarly journals Effects of Lacosamide Treatment on Epileptogenesis, Neuronal Damage and Behavioral Comorbidities in a Rat Model of Temporal Lobe Epilepsy

2021 ◽  
Vol 22 (9) ◽  
pp. 4667
Author(s):  
Michaela Shishmanova-Doseva ◽  
Dimitrinka Atanasova ◽  
Yordanka Uzunova ◽  
Lyubka Yoanidu ◽  
Lyudmil Peychev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Basolateral Amygdala ◽  
Neuronal Damage ◽  
Piriform Cortex ◽  
Preference Test ◽  
Neuroprotective Activity ◽  
Object Recognition Test ◽  
Beneficial Effects

Clinically, temporal lobe epilepsy (TLE) is the most prevalent type of partial epilepsy and often accompanied by various comorbidities. The present study aimed to evaluate the effects of chronic treatment with the antiepileptic drug (AED) lacosamide (LCM) on spontaneous motor seizures (SMS), behavioral comorbidities, oxidative stress, neuroinflammation, and neuronal damage in a model of TLE. Vehicle/LCM treatment (30 mg/kg, p.o.) was administered 3 h after the pilocarpine-induced status epilepticus (SE) and continued for up to 12 weeks in Wistar rats. Our study showed that LCM attenuated the number of SMS and corrected comorbid to epilepsy impaired motor activity, anxiety, memory, and alleviated depressive-like responses measured in the elevated plus maze, object recognition test, radial arm maze test, and sucrose preference test, respectively. This AED suppressed oxidative stress through increased superoxide dismutase activity and glutathione levels, and alleviated catalase activity and lipid peroxidation in the hippocampus. Lacosamide treatment after SE mitigated the increased levels of IL-1β and TNF-α in the hippocampus and exerted strong neuroprotection both in the dorsal and ventral hippocampus, basolateral amygdala, and partially in the piriform cortex. Our results suggest that the antioxidant, anti-inflammatory, and neuroprotective activity of LCM is an important prerequisite for its anticonvulsant and beneficial effects on SE-induced behavioral comorbidities.

scholarly journals Protective effects and mechanisms of high-dose vitamin C on sepsis-associated cognitive impairment in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ning Zhang ◽  
Wei Zhao ◽  
Zhen-Jie Hu ◽  
Sheng-Mei Ge ◽  
Yan Huo ◽  
...  
Keyword(s):  
Vitamin C ◽  
Escape Latency ◽  
Morris Water Maze Test ◽  
Protective Mechanism ◽  
High Dose ◽  
Maze Test ◽  
Tnf Α ◽  
Histopathologic Changes ◽  
High Dose Vitamin ◽  
Necrosis Factor

AbstractSepsis survivors present long-term cognitive deficits. The present study was to investigate the effect of early administration of high-dose vitamin C on cognitive function in septic rats and explore its possible cerebral protective mechanism. Rat sepsis models were established by cecal ligation and puncture (CLP). Ten days after surgery, the Morris water maze test was performed to evaluate the behavior and cognitive function. Histopathologic changes in the hippocampus were evaluated by nissl staining. The inflammatory cytokines, activities of antioxidant enzymes (superoxide dismutase or SOD) and oxidative products (malondialdehyde or MDA) in the serum and hippocampus were tested 24 h after surgery. The activity of matrix metalloproteinase-9 (MMP-9) and expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1(HO-1) in the hippocampus were measured 24 h after surgery. Compared with the sham group in the Morris water maze test, the escape latency of sepsis rats was significantly (P = 0.001) prolonged in the navigation test, whereas the frequency to cross the platform and the time spent in the target quadrant were significantly (P = 0.003) reduced. High-dose vitamin C significantly decreased the escape latency (P = 0.01), but increased the time spent in the target quadrant (P = 0.04) and the frequency to cross the platform (P = 0.19). In the CLP+ saline group, the pyramidal neurons were reduced and distributed sparsely and disorderly, the levels of inflammatory cytokines of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 in the serum and hippocampus were significantly increased (P = 0.000), the blood brain barrier (BBB) permeability in the hippocampus was significantly (P = 0.000) increased, the activities of SOD in the serum and hippocampus were significantly (P = 0.000 and P = 0.03, respectively) diminished while the levels of MDA in the serum and hippocampus were significantly (P = 0.007) increased. High-dose vitamin C mitigated hippocampus histopathologic changes, reduced systemic inflammation and neuroinflammation, attenuated BBB disruption, inhibited oxidative stress in brain tissue, and up-regulated the expression of nuclear and total Nrf2 and HO-1. High-dose vitamin C significantly (P < 0.05) decreased the levels of tumor necrosis factor- (TNF)-α, interleukin-6 (IL-6), MDA in the serum and hippocampus, and the activity of MMP-9 in the hippocampus, but significantly (P < 0.05) increased the levels of SOD, the anti-inflammatory cytokine (IL-10) in the serum and hippocampus, and nuclear and total Nrf2, and HO-1 in the hippocampus. In conclusion, high-dose vitamin C can improve cognition impairment in septic rats, and the possible protective mechanism may be related to inhibition of inflammatory factors, alleviation of oxidative stress, and activation of the Nrf2/HO-1 pathway.

scholarly journals 17β-Estradiol Modulates SIRT1 and Halts Oxidative Stress-Mediated Cognitive Impairment in a Male Aging Mouse Model

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 928 ◽  
Author(s):  
Mehtab Khan ◽  
Rahat Ullah ◽  
Shafiq Ur Rehman ◽  
Shahid Ali Shah ◽  
Kamran Saeed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Memory Impairment ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ros Generation ◽  
Dependent Manner ◽  
Molecular Docking Study ◽  
17Β Estradiol

Oxidative stress has been considered the main mediator in neurodegenerative disease and in normal aging processes. Several studies have reported that the accumulation of reactive oxygen species (ROS), elevated oxidative stress, and neuroinflammation result in cellular malfunction. These conditions lead to neuronal cell death in aging-related neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease. Chronic administration of d-galactose (d-gal) for a period of 10 weeks causes ROS generation and neuroinflammation, ultimately leading to cognitive impairment. In this study, we evaluated the estrogen receptor α (ERα)/silent mating type information regulation 2 homolog 1 (SIRT1)-dependent antioxidant efficacy of 17β-estradiol against d-gal-induced oxidative damage-mediated cognitive dysfunction in a male mouse model. The results indicate that 17β-estradiol, by stimulating ERα/SIRT1, halts d-gal-induced oxidative stress–mediated JNK/NF-ҡB overexpression, neuroinflammation and neuronal apoptosis. Moreover, 17β-estradiol ameliorated d-gal-induced AD-like pathophysiology, synaptic dysfunction and memory impairment in adult mouse brains. Interestingly, inhibition of SIRT1 with Ex527 (a potent and selective SIRT1 inhibitor) further enhanced d-gal-induced toxicity and abolished the beneficial effect of 17β-estradiol. Most importantly, for the first time, our molecular docking study reveals that 17β-estradiol allosterically increases the expression of SIRT1 and abolishes the inhibitory potential of d-ga. In summary, we can conclude that 17β-estradiol, in an ERα/SIRT1-dependent manner, abrogates d-gal-induced oxidative stress–mediated memory impairment, neuroinflammation, and neurodegeneration in adult mice.

scholarly journals Lactobacillus casei Strain Shirota Enhances the Ability of Geniposide to Activate SIRT1 and Decrease Inflammation and Oxidative Stress in Septic Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Chao Mai ◽  
Li Qiu ◽  
Yong Zeng ◽  
Xingqin Tan
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Lactobacillus Casei ◽  
P53 Protein ◽  
Cecal Ligation ◽  
Morris Water Maze Test ◽  
Gardenia Jasminoides ◽  
Tnf Α ◽  
Anti Oxidant ◽  
And Oxidative Stress

Gardenia jasminoides Ellis is rich in geniposide, which can be transformed into the anti-oxidant and anti-inflammatory agent genipin. Genipin exhibits greater efficacy than geniposide, but it is unstable and difficult to preserve. In this study, a mouse model for sepsis was established by cecal ligation and puncture, and then we explored the effects and mechanism of Lactobacillus casei strain Shirota (LcS) on the enhancement of the ability of geniposide to reduce sepsis and decrease inflammatory and oxidative levels in mice by the regulation of sirtuin type 1 (SIRT1). The mice were evaluated and analyzed by the open field test, Morris water maze test, flow cytometry, kit assay, qPCR, and western blot. The LcS + geniposide increased the survival rate in mice with sepsis, and increased the total travel distance, number of times the mice stood up, amount of time the mice spent grooming their fur, duration in the target quadrant, and crossing area number. The testing of mouse nerve cells showed that LcS + geniposide reduced the rate of nerve cell apoptosis caused by sepsis. LcS + geniposide also decreased the amount of inflammatory-related indicators of TNF-α, IL-6, and IL-1β, and the oxidation-related levels of malondialdehyde (MDA) in the hippocampi of septic mice, and it increased the oxidase activities of superoxide dismutase (SOD) and catalase (CAT). Additionally, LcS + geniposide increased the SOD1, SOD2, and CAT mRNA expression in the hippocampi of mice with sepsis and decreased the expression of TNF-α, IL-1β, NF-κB, and p53 mRNA. LcS+geniposide also increased the SIRT1 protein expression and decreased the Ac-FOXO1, Ac-NF-κB, and Ac-p53 protein expression in the hippocampi of mice with sepsis. We also observed that LcS + geniposide decreased the inflammatory and oxidative damage in the mice with sepsis. The effect of LcS + geniposide was similar to that of the drug dexamethasone and stronger than the effect of geniposide utilized alone. LcS also enhanced the ability of geniposide to activate SIRT1 and decrease the inflammation and oxidative stress in the septic mice, and it achieved an effect same with that obtained by the use of the drug dexamethasone.

scholarly journals Maternal Exposure to Sevoflurane Disrupts Oligodendrocyte Myelination of the Postnatal Hippocampus and Induces Cognitive and Motor Impairments in Offspring

2021 ◽  
Author(s):  
Ze Fan ◽  
Lirong Liang ◽  
Ruixue Ma ◽  
Rougang Xie ◽  
Youyi Zhao ◽  
...  
Keyword(s):  
Motor Coordination ◽  
Maternal Exposure ◽  
Morris Water Maze Test ◽  
The Novel ◽  
Motor Impairments ◽  
Object Recognition Test ◽  
Maze Test ◽  
Transmission Electron ◽  
Proliferation And Differentiation ◽  
Oligodendrocyte Precursor

Abstract Maternal exposure to sevoflurane can impose significant neurocognitive risks on the developing brain of infants. Several studies have indicated that oligodendrocytes may be involved in sevoflurane-induced neurotoxicity, but the concrete effects of sevoflurane on the development and myelination of oligodendrocytes remain unclear. In this study, we assessed fetal myelination and neural behavior after maternal exposure to sevoflurane. Pregnant C57BL/6J mice (gestational day 15.5) were exposed to sevoflurane (2.5%) for 6 h. The cognitive function and motor coordination of offspring (8 weeks of age) were determined via the novel object recognition test, the Morris water maze test and the accelerating rotarod test. Proliferation and differentiation of cultured oligodendrocyte precursor cells (OPCs) were detected via immunocytochemistry. Expression and ultrastructure of myelin in the fetal hippocampus were analyzed using immunohistochemistry and transmission electron microscopy (TEM). Myelin-associated genes and proteins were tested via qRT-PCR, immunofluorescence and western blotting. The functionality of myelin was evaluated by electrophysiology. The results showed that maternal exposure to sevoflurane induced cognitive and motor impairments in infants, accompanied by inhibitions of OPC proliferation and differentiation, and damages of myelin structure. Myelin-associated genes and proteins (including MBP, Olig1, PDNFRα, Sox10, etc.) were downregulated. The conduction velocity of axons also declined. These results suggested that maternal exposure to sevoflurane could induce detrimental effects on cognitive and motor functions in offspring, which might be associated with disrupted myelination of oligodendrocytes in the hippocampus.

scholarly journals Vinpocetine attenuates thioacetamide-induced liver fibrosis in rats

2020 ◽  
pp. 096032712094745
Author(s):  
Ahmed A Elnfarawy ◽  
Asmaa E Nashy ◽  
Alaa M Abozaid ◽  
Ibrahim F Komber ◽  
Rawan H Elweshahy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Vinca Alkaloid ◽  
Sprague Dawley ◽  
Ki 67 ◽  
Mortality And Morbidity ◽  
Beneficial Effects ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Synthetic Derivative

Liver fibrosis is associated with increased mortality and morbidity. However, there is not effective treatment so far. Vinpocetine (Vinpo) is a synthetic derivative of vinca alkaloid vincamine. Limited previous reports have shown some beneficial effects of Vinpo in different organ fibrosis, but the ability of Vinpo to inhibit liver fibrosis induced by thioacetamide (TAA) has not been reported, that is why we investigate the potential ability of this vinca alkaloid derivative to attenuate liver fibrosis. Hepatic fibrosis was induced in male Sprague Dawley rats by TAA (200 mg/kg; ip; 3 times/week) for 6 weeks. Daily treatments with Vinpo (10–20 mg/kg/day; orally) ameliorated TAA-induced hepatic oxidative stress and histopathological damage as indicated by a decrease in liver injury markers, LDH, hepatic MDA, and NOx levels, as well as increase anti-oxidative parameters. Besides, the anti-fibrotic efficacy of Vinpo was confirmed by decreasing hydroxyproline, and α-SMA. Also, the anti-inflammatory effect of Vinpo was explored by decreasing IL-6 and TNF-α levels. Our novel findings were that Vinpo decreased VEGF/Ki-67 expression in the liver confirming its effect on angiogenesis and proliferation. These findings reveal the anti-fibrotic effect of Vinpo against TAA-induced liver fibrosis in rats, and suggest the modulation of oxidative stress, inflammation, angiogenesis and proliferation as mechanistic cassette underlines this effect.

scholarly journals Thymus vulgaris Essential Oil Protects Zebrafish against Cognitive Dysfunction by Regulating Cholinergic and Antioxidants Systems

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1083 ◽  
Author(s):  
Luminita Capatina ◽  
Elena Todirascu-Ciornea ◽  
Edoardo Marco Napoli ◽  
Giuseppe Ruberto ◽  
Lucian Hritcu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Essential Oil ◽  
Ache Activity ◽  
Cholinergic Neurons ◽  
Thymus Vulgaris ◽  
Object Recognition Test ◽  
Memory Impairments ◽  
Beneficial Effects ◽  
Gas Chromatograph Mass Spectrometry ◽  
The Brain

Thymus vulgaris L. is an aromatic herb used for medicinal purposes such as antimicrobial, spasmolytic, antioxidant, anti-inflammatory, antinociceptive, antitumor, and may have beneficial effects in the treatment of Alzheimer’s disease. The present study aimed to investigate whether Thymus vulgaris L. essential oil enhances cognitive function via the action on cholinergic neurons using scopolamine (Sco)-induced zebrafish (Danio rerio) model of memory impairments. Thymus vulgaris L. essential oil (TEO, 25, 150, and 300 µL/L) was administered by immersion to zebrafish once daily for 13 days, whereas memory impairment was induced by Sco (100 μM), a muscarinic receptor antagonist, delivered 30 min before behavioral tests. Spatial memory was assessed using the Y-maze test and novel object recognition test (NOR). Anxiety and depression were measured in the novel tank diving test (NTT). Gas Chromatograph-Mass Spectrometry (GC-MS) analysis was used to study the phytochemical composition of TEO. Acetylcholinesterase (AChE) activity and oxidative stress response in the brain of zebrafish were determined. TEO ameliorated Sco-induced increasing of AChE activity, amnesia, anxiety, and reduced the brain antioxidant capacity. These results suggest that TEO may have preventive and/or therapeutic potentials in the management of memory deficits and brain oxidative stress in zebrafish with amnesia.

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