scholarly journals Metformin improves cognitive impairment in diabetic mice induced by a combination of streptozotocin and isoflurane anesthesia

Bioengineered ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 10982-10993
Author(s):  
Weiwei Zhang ◽  
Lingxia Zhao ◽  
Jianwen Zhang ◽  
Pengfei Li ◽  
Zhigan Lv
Keyword(s):  
Cognitive Impairment ◽  
Diabetic Mice ◽  
Isoflurane Anesthesia

scholarly journals Flos Puerariae Extract Ameliorates Cognitive Impairment in Streptozotocin-Induced Diabetic Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Zhong-he Liu ◽  
Hong-guang Chen ◽  
Pan-feng Wu ◽  
Qing Yao ◽  
Hong-ke Cheng ◽  
...  
Keyword(s):  
Body Weight ◽  
Cerebral Cortex ◽  
Cognitive Impairment ◽  
Cognitive Deficits ◽  
Ache Activity ◽  
Memory Deficits ◽  
Test Body ◽  
Morris Water Maze Test ◽  
Diabetic Mice ◽  
Mice Model

Objective. The effects of Flos Puerariae extract (FPE) on cognitive impairment associated with diabetes were assessed in C57BL/6J mice.Methods. Experimental diabetic mice model was induced by one injection of 50 mg/kg streptozotocin (STZ) for 5 days consecutively. FPE was orally administrated at the dosages of 50, 100, or 200 mg/kg/day, respectively. The learning and memory ability was assessed by Morris water maze test. Body weight, blood glucose, free fatty acid (FFA) and total cholesterol (TCH) in serum, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and acetylcholinesterase (AChE) activities in cerebral cortex and hippocampus were also measured.Results. Oral administration of FPE significantly improved cognitive deficits in STZ-induced diabetic mice. FPE treatment also maintained body weight and ameliorated hyperglycemia and dyslipidemia in diabetic mice. Additionally, decreased MDA level, enhanced CAT, and GSH-Px activities in cerebral cortex or hippocampus, as well as alleviated AChE activity in cerebral cortex, were found in diabetic mice supplemented with FPE.Conclusion. This study suggests that FPE ameliorates memory deficits in experimental diabetic mice, at least partly through the normalization of metabolic abnormalities, ameliorated oxidative stress, and AChE activity in brain.

Differential central pathology and cognitive impairment in pre-diabetic and diabetic mice

2013 ◽  
Vol 38 (11) ◽  
pp. 2462-2475 ◽  
Author(s):  
Juan Jose Ramos-Rodriguez ◽  
Oscar Ortiz ◽  
Margarita Jimenez-Palomares ◽  
Kevin R. Kay ◽  
Esther Berrocoso ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Diabetic Mice ◽  
Central Pathology

scholarly journals Gene-Specific DNA Methylation Linked to Postoperative Cognitive Dysfunction in Apolipoprotein E3 and E4 Mice

2021 ◽  
Vol 83 (3) ◽  
pp. 1251-1268
Author(s):  
Katie J. Schenning ◽  
Sarah Holden ◽  
Brett A. Davis ◽  
Amelia Mulford ◽  
Kimberly A. Nevonen ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cognitive Impairment ◽  
Postoperative Cognitive Dysfunction ◽  
Brain Regions ◽  
Epigenetic Modifications ◽  
Surgical Patients ◽  
Isoflurane Anesthesia ◽  
Genome Wide ◽  
Impaired Cognition ◽  
Postoperative Cognitive Impairment

Background: Geriatric surgical patients are at higher risk of developing postoperative neurocognitive disorders (NCD) than younger patients. The specific mechanisms underlying postoperative NCD remain unknown, but they have been linked to genetic risk factors, such as the presence of APOE4, compared to APOE3, and epigenetic modifications caused by exposure to anesthesia and surgery. Objective: To test the hypothesis that compared to E3 mice, E4 mice exhibit a more pronounced postoperative cognitive impairment associated with differential DNA methylation in brain regions linked to learning and memory. Methods: 16-month-old humanized apolipoprotein-E targeted replacement mice bearing E3 or E4 were subjected to surgery (laparotomy) under general isoflurane anesthesia or sham. Postoperative behavioral testing and genome-wide DNA methylation were performed. Results: Exposure to surgery and anesthesia impaired cognition in aged E3, but not E4 mice, likely due to the already lower cognitive performance of E4 prior to surgery. Cognitive impairment in E3 mice was associated with hypermethylation of specific genes, including genes in the Ephrin pathway implicated in synaptic plasticity and learning in adults and has been linked to Alzheimer’s disease. Other genes, such as the Scratch Family Transcriptional Repressor 2, were altered after surgery and anesthesia in both the E3 and E4 mice. Conclusion: Our findings suggest that the neurocognitive and behavioral effects of surgery and anesthesia depend on baseline neurocognitive status and are associated with APOE isoform-dependent epigenetic modifications of specific genes and pathways involved in memory and learning.

scholarly journals Minocycline Attenuates Cognitive Impairment Induced by Isoflurane Anesthesia in Aged Rats

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e61385 ◽  
Author(s):  
Feijuan Kong ◽  
Shuping Chen ◽  
Yuan Cheng ◽  
Leilei Ma ◽  
Huishun Lu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Aged Rats ◽  
Isoflurane Anesthesia

scholarly journals Increased extrasynaptic GluN2B expression is involved in cognitive impairment after isoflurane anesthesia

2016 ◽  
Vol 12 (1) ◽  
pp. 161-168 ◽  
Author(s):  
LUNXU LI ◽  
ZHENGQIAN LI ◽  
YIYUN CAO ◽  
DONGSHENG FAN ◽  
DEHUA CHUI ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Isoflurane Anesthesia

scholarly journals WS635 Attenuates the Anesthesia/Surgery-Induced Cognitive Impairment in Mice

2021 ◽  
Vol 13 ◽  
Author(s):  
Jiefu Lin ◽  
Fuyi Shen ◽  
Jing Lu ◽  
Feng Liang ◽  
Yiying Zhang ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Abdominal Surgery ◽  
Neurocognitive Disorder ◽  
Barnes Maze ◽  
Wild Type ◽  
Isoflurane Anesthesia ◽  
Before And After ◽  
Mice Brain ◽  
Different Doses

Anesthesia/surgery has been reported to be associated with perioperative neurocognitive disorder (PND) in patients and induces cognitive impairment in mice. Previous studies demonstrate cyclosporine A (CsA) attenuates the anesthesia/surgery-induced cognitive impairment in mice. However, CsA has immunosuppressive effects and may not be routinely used to prevent or treat PND in patients. WS635 is a nonimmunosuppressive CsA analog. We, therefore, set out to determine whether WS635 could mitigate the anesthesia/surgery-induced cognitive impairment in mice. We performed abdominal surgery under 1.4% isoflurane anesthesia (anesthesia/surgery) for 2 h in 9 month-old wild-type (WT) mice. We treated the mice with CsA (10 mg/kg) or different doses (13.2 mg/kg, 26.4 mg/kg and 52.8 mg/kg) of WS635 before and after the anesthesia/surgery. Barnes maze and fear conditioning system (FCS) were employed to evaluate the cognitive function in mice. We measured the amounts of postsynaptic density (PSD)-95, synaptophysin, and ATP in the hippocampus and cortex of the mice using western blot and ATP Colorimetric/Fluorometric Assay, respectively. We found that the treatment with 52.8 mg/kg, but not 13.2 mg/kg or 26.4 mg/kg, of WS635 attenuated the anesthesia/surgery-induced cognitive impairment in mice and the reductions in the amounts of PSD-95, synaptophysin, and ATP in the mice brain tissues. These results have established a system to study WS635 further and suggest that we need to perform more experiments to determine whether WS635 can ultimately be used as one of the interventions for PND in patients.

scholarly journals Bactericidal/Permeability-Increasing Protein Improves Cognitive Impairment in Diabetic Mice via Blockade of the LPS-LBP-TLR4 Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Qin Sun ◽  
Tingxin Li ◽  
Yamei Li ◽  
Lingling Wei ◽  
Min Zhang ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Signaling Pathway ◽  
Tissue Injury ◽  
Fasting Blood Glucose ◽  
Serum Levels ◽  
Diabetic Mice ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway ◽  
Glucose Plasma ◽  
Lps Treatment

Emerging evidence suggests that the bactericidal/permeability-increasing protein (BPI) is involved in the process of cognitive impairment in diabetes. However, its underlying mechanism remains elusive. In this study, we found that BPI affects cognitive impairment due to diabetes through the lipopolysaccharide (LPS)-lipopolysacharide-binding protein (LBP)-toll-like receptor 4 (TLR4) signaling pathway. We examined the expression of BPI, LPS, LBP, CD14, and TLR4 in established mouse models of diabetes induced by high-fat diet (HFD) in combination with streptozotocin (STZ). Diabetic mice were then injected with adeno-associated-virus carrying BPI overexpression vectors and LPS. Fasting blood glucose, plasma insulin, and serum levels of inflammatory factors were examined. Then, glucose tolerance and, insulin resistance tests were used to measure systemic insulin sensitivity. Next, hippocampal tissue injury and cell apoptosis were examined by hematoxylin-eosin (HE) and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining. Diabetic mice displayed increased LPS expression and activation of the LPS-CD14-TLR4 signaling pathway. HFD mice following LPS treatment showed significantly increased serum levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, and expressions of Bcl-2-associated X protein (Bax) and Aβ but decreased expression of Bcl-2 in hippocampal tissues, as well as enhanced fasting blood glucose, plasma insulin, glucose tolerance, insulin tolerance, cell apoptosis, aggravated hippocampal tissue injury and, ultimately, cognitive impairment. However, overexpression of BPI was able to rescue the aforementioned phenotypes driven by LPS treatment. Taken together, BPI could potentially provide relief from cognitive impairment in diabetic mice by disrupting the LPS-LBP-TLR4 signaling pathway, underscoring a possible alternative therapeutic strategy against the cognitive impairment associated with diabetes.

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