scholarly journals Environmental Enrichment Attenuated Sevoflurane-Induced Neurotoxicity through the PPAR-γSignaling Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Yupeng Zhao ◽  
Kaizheng Chen ◽  
Xia Shen
Keyword(s):  
Signaling Pathway ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Neuronal Apoptosis ◽  
Environmental Enrichment ◽  
Memory Function ◽  
Critical Role ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Peroxisome Proliferator ◽  
Young Mice

Sevoflurane is the most widely used inhaled anesthetic. Environmental enrichment (EE) can reverse sevoflurane-induced learning and memory impairment in young mice. However, the mechanism by which EE elicits this effect is unclear. The peroxisome proliferator-activated receptor (PPAR) regulatory pathway plays a critical role in the regulation of inflammation in central nervous system diseases. In this study, we investigated whether EE attenuates sevoflurane-induced learning and memory disability via the PPAR signaling pathway. Six-day-old mice were treated with 3% sevoflurane for 2 hours daily from postnatal day 6 (P6) to P8. Then, the mice were treated with EE. The effects of sevoflurane on learning and memory function, PPAR-γexpression in the brain, and the numbers of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells and 5-bromodeoxyuridine-positive cells in the hippocampus were determined. Sevoflurane induced neuronal apoptosis and neurogenesis inhibition, which may impair learning and memory in young mice. Furthermore, sevoflurane downregulated PPAR-γexpression. Both EE and the PPAR-γagonist, rosiglitazone, attenuated sevoflurane-induced neuronal apoptosis, neurogenesis inhibition, and learning and memory impairment. Our findings suggest that EE ameliorated sevoflurane-induced neurotoxicity and learning and memory impairment through the PPAR-γsignaling pathway. PPAR-γmay be a potential therapeutic target for preventing or treating sevoflurane-induced neurotoxicity.

Effects of Gossypium herbaceam Extract Administration on the Learning and Memory Function in the Naturally Aged Rats: Neuronal Niche Improvement1

2012 ◽  
Vol 31 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Yanyong Liu ◽  
Haji Akber Aisa ◽  
Chao Ji ◽  
Nan Yang ◽  
Haibo Zhu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Neuroprotective Effect ◽  
Memory Function ◽  
Aged Rats

Aging-associated cognitive impairment is an important health care issue since individuals with mild cognitive impairment are more likely to develop Alzheimer’s disease. In the present study, the protective effect of Gossypium herbaceam extracts (GHE) on learning and memory impairment associated with aging were examined in vivo using Morris water maze and step through task. Furthermore, the antioxidant activity and neuroprotective effect of GHE was investigated with methods of histochemistry and biochemistry. These data showed that oral administration with GHE at the doses of 35, 70, and 140 mg/kg exerted an improved effect on the learning and memory impairment in aged rats. Subsequently, GHE afforded a beneficial action on eradication of free radicals without influence on the activity of glutathione peroxidase and superoxide dismutase. GHE treatment enhanced the expression levels of nerve growth factor. Meanwhile, proliferation of neural progenitor cells was elevated in hippocampus after treatment with GHE. Taken together, neurogenic niche improvement could be involved in the mechanism underlying neuroprotection of GHE against aging-associated cognitive impairment. These findings suggested that GHE might be a potential agent as cognitive-enhancing drugs that delay or halt mild cognitive impairment progression to Alzheimer’s disease or treatment of aging-associated cognitive impairment.

scholarly journals Impact of Ketamine on Learning and Memory Function, Neuronal Apoptosis and Its Potential Association with miR-214 and PTEN in Adolescent Rats

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e99855 ◽  
Author(s):  
Ji Wang ◽  
Min Zhou ◽  
Xiaobin Wang ◽  
Xiaoling Yang ◽  
Maohua Wang ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Neuronal Apoptosis ◽  
Memory Function ◽  
Potential Association ◽  
Adolescent Rats

scholarly journals Effects of Caloric Intake on Learning and Memory Function in Juvenile C57BL/6J Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Bao-Lei Xu ◽  
Rong Wang ◽  
Li-Na Ma ◽  
Wen Dong ◽  
Zhi-Wei Zhao ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Function ◽  
Caloric Intake ◽  
Camp Response Element Binding ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Downstream Effectors ◽  
Element Binding Protein

Dietary composition may influence neuronal function as well as processes underlying synaptic plasticity. In this study, we aimed to determine the effect of high and low caloric diets on a mouse model of learning and memory and to explore mechanisms underlying this process. Mice were divided into three different dietary groups: normal control(n=12), high-caloric (HC) diet(n=12), and low-caloric (LC) diet(n=12). After 6 months, mice were evaluated on the Morris water maze to assess spatial memory ability. We found that HC diet impaired learning and memory function relative to both control and LC diet. The levels of SIRT1 as well as its downstream effectors p53, p16, and peroxisome proliferator-activated receptorγ(PPARγ) were decreased in brain tissues obtained from HC mice. LC upregulated SIRT1 but downregulated p53, p16, and PPARγ. The expressions of PI3K and Akt were not altered after HC or LC diet treatment, but both LC and HC elevated the levels of phosphorylated-cAMP response element-binding protein (p-CREB) and IGF-1 in hippocampal CA1 region. Therefore, HC diet-induced dysfunction in learning and memory may be prevented by caloric restriction via regulation of the SIRT1-p53 or IGF-1 signaling pathways and phosphorylation of CREB.

PKA-CREB-BDNF signaling pathway mediates propofol-induced long-term learning and memory impairment in hippocampus of rats

2018 ◽  
Vol 1691 ◽  
pp. 64-74 ◽  
Author(s):  
Yu Zhong ◽  
Jing Chen ◽  
Li Li ◽  
Yi Qin ◽  
Yi Wei ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Bdnf Signaling

scholarly journals Neuroprotective Effect of Danggui Shaoyao San via the Mitophagy-Apoptosis Pathway in a Rat Model of Alzheimer’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zhenyan Song ◽  
Deyong Luo ◽  
Yuke Wang ◽  
Yushan Zheng ◽  
Peiying Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Neuronal Apoptosis ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Morris Water Maze Test ◽  
High Dose ◽  
Sham Operation ◽  
Apoptosis Pathway ◽  
Model Of Alzheimer’S Disease

Alzheimer’s disease (AD) is a serious neurodegenerative disease. While the main pathological characteristic of AD is widely believed to be the accumulation of amyloid-beta (Aβ) in neurons around neurofibrillary plaques, the molecular mechanism of pathological changes is not clear. Traditional Chinese medicine offers many treatments for AD. Among these, Danggui Shaoyao San (DSS) is a classic prescription. In this study, an AD model was established by injecting Aβ 1–42 into the brains of rats, which were then treated with different concentrations of Danggui Shaoyao San (sham operation; model; and Danggui Shaoyao San high-dose, medium-dose, and low-dose intervention groups). The Morris water maze test was used to assess the learning and memory abilities of the animals in each group. Nissl staining was used to detect neurons. Mitophagy was evaluated by transmission electron microscopy and immunofluorescence colocalization. Apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression levels of autophagy- and apoptosis-related proteins were measured by western blot. Compared to the model group, the groups of AD rats administered medium and high doses of Danggui Shaoyao San showed significantly increased learning and memory abilities ( P < 0.05 ), as well as significantly increased autophagosomes in the hippocampus. Moreover, the expression of PTEN-induced kinase 1 (PINK1), Parkin, and microtubule-associated protein light chain 3 (LC3-I/LC3-II) was increased, while that of p62 was significantly decreased ( P < 0.05 ). The neuronal apoptosis rate was also significantly decreased, the Bcl-2/Bax ratio was significantly increased, and the cleaved caspase-3 protein expression was significantly decreased ( P < 0.05 ). Therefore, Danggui Shaoyao San inhibited neuronal apoptosis in AD rats via a mechanism that may be related to the activation of the PINK1-Parkin-mediated mitophagy signaling pathway.

scholarly journals Interventional Effects of DHA on Behavioral Memory Impairment Caused by Repeated Anesthesia of Sevoflurane in Aged Rats

2020 ◽  
Author(s):  
Ming Tian ◽  
Kezhong Li ◽  
Xiaoling Zhao
Keyword(s):  
Signaling Pathway ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Escape Latency ◽  
Control Group ◽  
High Dose ◽  
Group Model ◽  
Aged Rats ◽  
Sevoflurane Anesthesia ◽  
Behavioral Memory

Abstract Backgroud: The current study aimed to explore the effects of Docosahexaenoic acid (DHA) on the behavioral memory impairment induced by repeated anesthesia of sevoflurane in aged rats. Methods: A total of 45 Sprague‑Dawley (SD) aged rats were randomly divided into five groups: Blank control group (Control), sevoflurane group (Model), low-dose DHA group (L-DHA; 0.3g/kg), medium-dose DHA group (M-DHA; 1g/kg) and high-dose DHA group (H-DNA; 3g/kg). Morris water maze experiment was used to evaluate the learning and memory ability of rats. Hematoxylin and eosin staining was used to observe histological changes in the hippocampus. Immunohistochemistry and western blot analysis were used to determine the expression of the Nuclear factor erythroid-2 (NF-E2)-related factor 2(Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway. Results: Rats were indicated to exhibit prolonged escape latency following sevoflurane anesthesia. The number of times taken to cross the platform and the time for target quadrant stay were also demonstrated to be significantly reduced. Rats treated with different doses of DHA were revealed to exhibit reduced escape latency. The number of times taken to cross the platform and the time for target quadrant stay increased. Histopathological examination indicated that DHA attenuated the brain function of the rats that were repeatedly anesthetized using sevoflurane. Furthermore, the expression of Nrf2 and HO-1 protein were demonstrated to be significantly increased. Conclusions: The present study revealed that DHA has a protective effect on learning and memory impairment in aged rats induced by repeated sevoflurane anesthesia, and the mechanism may be associated with the Nrf2/HO-1 signaling pathway.

scholarly journals SerpinA3N deficiency deteriorates impairments of learning and memory in mice following hippocampal stab injury

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Zhi-Meng Wang ◽  
Cong Liu ◽  
Ying-Ying Wang ◽  
Yu-Sen Deng ◽  
Xuan-Cheng He ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Hippocampal Neurons ◽  
Neuronal Apoptosis ◽  
Early Stage ◽  
Critical Role ◽  
Specific Inhibitor ◽  
Serine Protease Inhibitor ◽  
Therapeutic Agents ◽  
Spatial Learning And Memory ◽  
Stab Injury

Abstract Traumatic brain injury is a global leading cause of disability and death, which puts patients at high risk for developing dementia. Early intervention is believed as the key to minimize the development of brain damages that could aggravate the symptoms. Here, we report that the serine protease inhibitor SerpinA3N is upregulated in hippocampal neurons in the early stage of hippocampal stab injury (HSI), while its deficiency causes a greater degree of neuronal apoptosis and severer impairments of spatial learning and memory in mice after HSI. We further show that MMP2 is a key substrate of SerpinA3N, and MMP2 specific inhibitor (ARP100) can protect against neuronal apoptosis and cognitive dysfunction in mice after HSI. These findings demonstrate a critical role for SerpinA3N in neuroprotection, suggesting that SerpinA3N and MMP2 inhibitors might be a novel therapeutic agents for neurotrauma.

scholarly journals Sevoflurane Induces Learning and Memory Impairment in Young Mice Through a Reduction in Neuronal Glucose Transporter 3

2019 ◽  
Vol 40 (6) ◽  
pp. 879-895
Author(s):  
Jinpiao Zhu ◽  
Zongze Zhang ◽  
Junke Jia ◽  
Lirong Wang ◽  
Qiuyue Yang ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Learning And Memory ◽  
Temporal Lobe ◽  
Hippocampal Neurons ◽  
Memory Impairment ◽  
Glucose Transporter ◽  
Sevoflurane Anaesthesia ◽  
Gene And Protein Expression ◽  
Young Mice

AbstractSevoflurane, which is widely used in paediatric anaesthesia, induces neural apoptosis in the developing brain and cognitive impairment in young mammals. Glucose hypometabolism is the key pathophysiological modulator of cognitive dysfunction. However, the effects and mechanism of sevoflurane on cerebral glucose metabolism after its use as an anaesthetic and its complete elimination are still unknown. We therefore investigated the influence of sevoflurane on neuronal glucose transporter isoform 3 (GLUT3) expression, glucose metabolism and apoptosis in vivo and in vitro and on neurocognitive function in young mice 24 h after the third exposure to sevoflurane. Postnatal day 14 (P14) mice and neural cells were exposed to 3% sevoflurane 2 h daily for three days. We found that sevoflurane anaesthesia decreased GLUT3 gene and protein expression in the hippocampus and temporal lobe, consistent with a decrease in glucose metabolism in the hippocampus and temporal lobe observed by [18F] fluorodeoxyglucose positron emission tomography (18F-FDG PET). Moreover, sevoflurane anaesthesia increased the number of TUNEL-positive cells and the levels of Bax, cleaved caspase 3 and cleaved PARP and reduced Bcl-2 levels in the hippocampus and temporal lobe. Young mice exposed to sevoflurane multiple times also showed learning and memory impairment. In addition, sevoflurane inhibited GLUT3 expression in primary hippocampal neurons and PC12 cells. GLUT3 overexpression in cultured neurons ameliorated the sevoflurane-induced decrease in glucose utilization and increase in the apoptosis rate. These data indicate that GLUT3 deficiency may contribute to sevoflurane-induced learning and memory deficits in young mice.

scholarly journals Proinflammatory Factors Mediate Paclitaxel-Induced Impairment of Learning and Memory

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Zhao Li ◽  
Shuang Zhao ◽  
Hai-Lin Zhang ◽  
Peng Liu ◽  
Fei-Fei Liu ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Neuronal Apoptosis ◽  
Memory Function ◽  
Interleukin 1 ◽  
Spatial Learning And Memory ◽  
Synthesis Inhibitor ◽  
Expression Levels ◽  
Proinflammatory Factor ◽  
Paclitaxel Treatment

The chemotherapeutic agent paclitaxel is widely used for cancer treatment. Paclitaxel treatment impairs learning and memory function, a side effect that reduces the quality of life of cancer survivors. However, the neural mechanisms underlying paclitaxel-induced impairment of learning and memory remain unclear. Paclitaxel treatment leads to proinflammatory factor release and neuronal apoptosis. Thus, we hypothesized that paclitaxel impairs learning and memory function through proinflammatory factor-induced neuronal apoptosis. Neuronal apoptosis was assessed by TUNEL assay in the hippocampus. Protein expression levels of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in the hippocampus tissue were analyzed by Western blot assay. Spatial learning and memory function were determined by using the Morris water maze (MWM) test. Paclitaxel treatment significantly increased the escape latencies and decreased the number of crossing in the MWM test. Furthermore, paclitaxel significantly increased the number of TUNEL-positive neurons in the hippocampus. Also, paclitaxel treatment increased the expression levels of TNF-αand IL-1βin the hippocampus tissue. In addition, the TNF-αsynthesis inhibitor thalidomide significantly attenuated the number of paclitaxel-induced TUNEL-positive neurons in the hippocampus and restored the impaired spatial learning and memory function in paclitaxel-treated rats. These data suggest that TNF-αis critically involved in the paclitaxel-induced impairment of learning and memory function.

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