scholarly journals Appropriate exercise level attenuates gut dysbiosis and valeric acid increase to improve neuroplasticity and cognitive function after surgery in mice

2021 ◽  
Author(s):  
Zhongmeng Lai ◽  
Weiran Shan ◽  
Jun Li ◽  
Jia Min ◽  
Xianzhang Zeng ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gut Microbiota ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Postoperative Cognitive Dysfunction ◽  
Valeric Acid ◽  
Low Intensity ◽  
Adult Mice ◽  
Low Intensity Exercise ◽  
Old Mice

AbstractPostoperative cognitive dysfunction (POCD) affects the outcome of millions of patients each year. Aging is a risk factor for POCD. Here, we showed that surgery induced learning and memory dysfunction in adult mice. Transplantation of feces from surgery mice but not from control mice led to learning and memory impairment in non-surgery mice. Low intensity exercise improved learning and memory in surgery mice. Exercise attenuated surgery-induced neuroinflammation and decrease of gut microbiota diversity. These exercise effects were present in non-exercise mice receiving feces from exercise mice. Exercise reduced valeric acid, a gut microbiota product, in the blood. Valeric acid worsened neuroinflammation, learning and memory in exercise mice with surgery. The downstream effects of exercise included attenuating growth factor decrease, maintaining astrocytes in the A2 phenotypical form possibly via decreasing C3 signaling and improving neuroplasticity. Similar to these results from adult mice, exercise attenuated learning and memory impairment in old mice with surgery. Old mice receiving feces from old exercise mice had better learning and memory than those receiving control old mouse feces. Surgery increased blood valeric acid. Valeric acid blocked exercise effects on learning and memory in old surgery mice. Exercise stabilized gut microbiota, reduced neuroinflammation, attenuated growth factor decrease and preserved neuroplasticity in old mice with surgery. These results provide direct evidence that gut microbiota alteration contributes to POCD development. Valeric acid is a mediator for this effect and a potential target for brain health. Low intensity exercise stabilizes gut microbiota in the presence of insult, such as surgery.

scholarly journals A Long-Term Enriched Environment Ameliorates the Accelerated Age-Related Memory Impairment Induced by Gestational Administration of Lipopolysaccharide: Role of Plastic Mitochondrial Quality Control

2021 ◽  
Vol 14 ◽  
Author(s):  
Zhan-Qiang Zhuang ◽  
Zhe-Zhe Zhang ◽  
Yue-Ming Zhang ◽  
He-Hua Ge ◽  
Shi-Yu Sun ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Memory Impairment ◽  
Spatial Learning And Memory ◽  
Mitochondrial Quality Control ◽  
Protein Levels ◽  
Age Related ◽  
Old Mice ◽  
Lps Treatment

Studies have shown that gestational inflammation accelerates age-related memory impairment in mother mice. An enriched environment (EE) can improve age-related memory impairment, whereas mitochondrial dysfunction has been implicated in the pathogenesis of brain aging. However, it is unclear whether an EE can counteract the accelerated age-related memory impairment induced by gestational inflammation and whether this process is associated with the disruption of mitochondrial quality control (MQC) processes. In this study, CD-1 mice received daily intraperitoneal injections of lipopolysaccharide (LPS, 50 μg/kg) or normal saline (CON group) during gestational days 15–17 and were separated from their offspring at the end of normal lactation. The mothers that received LPS were divided into LPS group and LPS plus EE (LPS-E) treatment groups based on whether the mice were exposed to an EE until the end of the experiment. At 6 and 18 months of age, the Morris water maze test was used to evaluate spatial learning and memory abilities. Quantitative reverse transcription polymerase chain reaction and Western blot were used to measure the messenber RNA (mRNA) and protein levels of MQC-related genes in the hippocampus, respectively. The results showed that all the aged (18 months old) mice underwent a striking decline in spatial learning and memory performances and decreased mRNA/protein levels related to mitochondrial dynamics (Mfn1/Mfn2, OPA1, and Drp1), biogenesis (PGC-1α), and mitophagy (PINK1/parkin) in the hippocampi compared with the young (6 months old) mice. LPS treatment exacerbated the decline in age-related spatial learning and memory and enhanced the reduction in the mRNA and protein levels of MQC-related genes but increased the levels of PGC-1α in young mice. Exposure to an EE could alleviate the accelerated decline in age-related spatial learning and memory abilities and the accelerated changes in MQC-related mRNA or protein levels resulting from LPS treatment, especially in aged mice. In conclusion, long-term exposure to an EE can counteract the accelerated age-related spatial cognition impairment modulated by MQC in CD-1 mother mice that experience inflammation during pregnancy.

scholarly journals Neuroinflammation Induced by Surgery Does Not Impair the Reference Memory of Young Adult Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Yanhua Zhao ◽  
Lili Huang ◽  
Huan Xu ◽  
Guangxi Wu ◽  
Mengyi Zhu ◽  
...  
Keyword(s):  
Risk Factor ◽  
Young Adult ◽  
Postoperative Cognitive Dysfunction ◽  
Underlying Mechanism ◽  
Reference Memory ◽  
Behavior Changes ◽  
Spatial Reference ◽  
Adult Mice ◽  
Spatial Reference Memory ◽  
Old Mice

Postoperative cognitive dysfunction (POCD) increases morbidity and mortality after surgery. But the underlying mechanism is not clear yet. While age is now accepted as the top one risk factor for POCD, results from studies investigating postoperative cognitive functions in adults have been controversial, and data about the very young adult individuals are lacking. The present study investigated the spatial reference memory, IL-1β, IL-6, and microglia activation changes in the hippocampus in 2-month-old mice after anesthesia and surgery. We found that hippocampal IL-1βand IL-6 increased at 6 hours after surgery. Microglia were profoundly activated in the hippocampus 6 to 24 hours after surgery. However, no significant behavior changes were found in these mice. These results indicate that although anesthesia and surgery led to neuroinflammation, the latter was insufficient to impair the spatial reference memory of young adult mice.

Low-intensity exercise training maintains adipokines in obese children

2010 ◽  
Vol 01 (01) ◽  
pp. 017-022
Author(s):  
Sunghwun Kang ◽  
Jinhee Woo ◽  
Nam-Hwoeh Yeo ◽  
Duckpil Ok ◽  
Jaeho Yoo ◽  
...  
Keyword(s):  
Body Composition ◽  
Growth Factors ◽  
Growth Factor ◽  
Exercise Training ◽  
Body Fat ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Obese Children ◽  
Low Intensity ◽  
Low Intensity Exercise

AbstractThe aim of the present study is to investigate the effects of a 12 weeks low-intensity exercise training on body composition, adipokines, and growth factors in normal (NG) and obese (OG) children. Maximal oxygen uptake (VO2max); body composition; adipokines consisting of adiponectin, retinol binding protein-4 (RBP4), and interleukin-6 (IL-6); and growth factors including insulin like growth factor-1 (IGF-1) and insulin like growth factor binding protein-3 (IGF-BP3) were measured before and after low-intensity exercise training program. Body composition parameters such as body weight, body mass index, body fat (%) and VO2 max were significantly different between NG and OG. Adiponectin levels in NG were increased after 12 weeks exercise training. In addition, our results showed that the concentrations of adiponectin, RBP4, IGF-1, and IGF-BP3 in OG were higher than those of NG. Adiponectin levels were significantly correlated with body fat (r = −0.545, p = 0.001) and VO2max (r = 0.368, p = 0.032) and RBP4 levels were significantly correlated with body fat (r = 0.371, p = 0.031) in all subjects. Exercise training improved adiponectin levels in NG subjects and maintained the levels of body fat, adipokines (adiponectin, RBP4), and growth factors (IGF-1, IGF-BP3) in OG subjects. The present study revealed that regular low-intensity exercise training is strongly associated with high adiponectin levels in healthy children. However, obese children did not exhibit any changes in the levels of adipokines and maintained body composition and growth factors.

Effect of hormones on hydrolase activities and DNA synthesis in kidney of the developing mouse

1988 ◽  
Vol 66 (5) ◽  
pp. 580-585 ◽  
Author(s):  
Normand Brière
Keyword(s):  
Alkaline Phosphatase ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Mouse Kidney ◽  
Adult Mice ◽  
Cortisone Injection ◽  
Epidermal Growth ◽  
Brush Border Enzyme ◽  
Old Mice

The postnatal development of brush border enzyme activities, namely maltase, trehalase, alkaline phosphatase, γ-glutamyltranspeptidase, and leucylnaphthylamidase, as well as the ontogenic profile of DNA synthesis has been determined in the mouse kidney. In addition, these parameters were evaluated following daily administration of hormones during 3 days to 8-day-old mice. Insulin or epidermal growth factor induced a 34% increase of maltase activity over that of 11-day-old controls. Trehalase activity was precociously and significantly augmented by cortisone alone or combined with thyroxine (p < 0.05), although thyroxine alone had no influence. Only epidermal growth factor had a significant effect on alkaline phosphatase activity. γ-Glutamyltranspeptidase activity was significantly decreased when insulin and thyroxine were given simultaneously, but was not modified by any of the hormones injected separately. The level of leucylnaphthylamidase activity was enhanced by 70% after cortisone injection, but it was significantly reduced by thyroxine injected in combination with insulin or cortisone. The incorporation of [3H]thymidine into DNA was increased by 107% after epidermal growth factor administration, but it was decreased by 33% after the cortisone treatment. In spite of this precocious reduction, the level of incorporation was still 2 times higher than that in adult mice. These results show that hormones act separately or in cooperation to accelerate or retard the maturation of the suckling mouse kidney.

Transforming growth factor-β in the brain is activated by exercise and increases mobilization of fat-related energy substrates in rats

2007 ◽  
Vol 292 (5) ◽  
pp. R1851-R1861 ◽  
Author(s):  
Tetsuro Shibakusa ◽  
Wataru Mizunoya ◽  
Yuki Okabe ◽  
Shigenobu Matsumura ◽  
Yoko Iwaki ◽  
...  
Keyword(s):  
Nervous System ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Ketone Bodies ◽  
Nonesterified Fatty Acid ◽  
Energy Substrates ◽  
Low Intensity ◽  
Related Energy ◽  
Low Intensity Exercise ◽  
The Brain

We have recently reported that inhibition of transforming growth factor (TGF)-β in the brain reduced fat-related energy substrates concentrations in response to exercise. We investigated the relevance between the mobilization of fat-related energy substrates (nonesterified fatty acid and ketone bodies) during exercise and the effects of TGF-β in the brain. Low-intensity exercise was simulated by contraction of the hindlimbs, induced by electrical stimulation at 2 Hz in anesthetized rats (Sim-Ex). As with actual exercise, it was confirmed that mobilization of carbohydrate-related energy substrates (glucose and lactic acid) occurred immediately after the onset of Sim-Ex, and mobilization of fat-related energy substrates followed thereafter. The timing of mobilization of fat-related substrates corresponded to that of the increase in TGF-β in cerebrospinal fluid (CSF) in Sim-Ex. The level of TGF-β in CSF significantly increased after 10 min of Sim-Ex and remained elevated until 30 min of Sim-Ex. Intracisternal administration of TGF-β caused rapid mobilization of fat-related energy substrates. Meanwhile, there were no effects on the changes in carbohydrate-related substrates. The levels of catecholamines were slightly elevated after TGF-β administration, and, although not significantly in statistical terms, we consider that at least a part of TGF-β signal was transducted via the sympathetic nervous system because of these increases. These data indicate that TGF-β in the brain is closely related to the mobilization of fat-related energy substrates during low-intensity exercise. We hypothesized that the central nervous system plays a role in the regulation of energy metabolism during low-intensity exercise and this may be mediated by TGF-β.

Surgery Trauma Severity but not Anesthesia Length Contributes to Postoperative Cognitive Dysfunction in Mice

2021 ◽  
pp. 1-13
Author(s):  
Zhongmeng Lai ◽  
Jia Min ◽  
Jun Li ◽  
Weiran Shan ◽  
Weifeng Yu ◽  
...  
Keyword(s):  
Object Recognition ◽  
Learning And Memory ◽  
Postoperative Cognitive Dysfunction ◽  
Surgical Trauma ◽  
Novel Object Recognition ◽  
Barnes Maze ◽  
Novel Object ◽  
Isoflurane Anesthesia ◽  
Modifiable Factors ◽  
Old Mice

Background: Perioperative, modifiable factors contributing to perioperative neurocognitive disorders (PND) have not been clearly defined. Objective: To determine the contribution of anesthesia lengths and the degrees of surgical trauma to PND and neuroinflammation, a critical process for PND. Methods: Three-month-old C57BL/6J mice were subjected to 2 h or 6 h isoflurane anesthesia plus a 5 min or 15 min left common carotid artery exposure (surgery) in a factorial design (two factors: anesthesia with two levels and surgery with three levels). Their learning and memory were tested by Barnes maze and novel object recognition paradigms. Blood, spleen, and hippocampus were harvested for measuring interleukin (IL)-6 and IL-1β. Eighteen-month-old C57BL/6J mice (old mice) were subjected to 6 h isoflurane anesthesia or 2 h isoflurane anesthesia plus 15 min surgery and then had learning and memory tested. Results: Three-month-old mice with 15 min surgery (long surgery) under 2 h or 6 h anesthesia performed poorly in the learning and memory tests compared with controls. Anesthesia alone or anesthesia plus 5 min surgery did not affect mouse performance in these tests. Similarly, only mice with long surgery but not mice with other experimental conditions had increased IL-6 and IL-1β in the blood, spleen, and hippocampus and decreased spleen weights. Splenocytes were found in the hippocampus after surgery. Similarly, old mice with long surgery but not the mice with isoflurane anesthesia alone had poor performance in the Barnes maze and novel object recognition tests. Conclusion: Surgical trauma, but not anesthesia, contributes to the development of PND and neuroinflammation. Splenocytes may modulate these processes.

scholarly journals Aging-Induced Dysbiosis of Gut Microbiota as a Risk Factor for Increased Listeria monocytogenes Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Mohammad S. Alam ◽  
Jayanthi Gangiredla ◽  
Nur A. Hasan ◽  
Tammy Barnaba ◽  
Carmen Tartera
Keyword(s):  
Listeria Monocytogenes ◽  
Young Adult ◽  
Gut Microbiota ◽  
Dna Sequences ◽  
Post Infection ◽  
Bacterial Species ◽  
Case Fatality ◽  
Adult Mice ◽  
Α Diversity ◽  
Old Mice

Invasive foodborne Listeria monocytogenes infection causes gastroenteritis, septicemia, meningitis, and chorioamnionitis, and is associated with high case-fatality rates in the elderly. It is unclear how aging alters gut microbiota, increases risk of listeriosis, and causes dysbiosis post-infection. We used a geriatric murine model of listeriosis as human surrogate of listeriosis for aging individuals to study the effect of aging and L. monocytogenes infection. Aging and listeriosis-induced perturbation of gut microbiota and disease severity were compared between young-adult and old mice. Young-adult and old mice were dosed intragastrically with L. monocytogenes. Fecal pellets were collected pre- and post-infection for microbiome analysis. Infected old mice had higher Listeria colonization in liver, spleen, and feces. Metagenomics analyses of fecal DNA-sequences showed increase in α-diversity as mice aged, and infection reduced its diversity. The relative abundance of major bacterial phylum like, Bacteroidetes and Firmicutes remained stable over aging or infection, while the Verrucomicrobia phylum was significantly reduced only in infected old mice. Old mice showed a marked reduction in Clostridaiceae and Lactobacillaceae bacteria even before infection when compared to uninfected young-adult mice. L. monocytogenes infection increased the abundance of Porphyromonadaceae and Prevotellaceae in young-adult mice, while members of the Ruminococcaceae and Lachnospiraceae family were significantly increased in old mice. The abundance of the genera Blautia and Alistipes were significantly reduced post-infection in young-adult and in old mice as compared to their uninfected counterparts. Butyrate producing, immune-modulating bacterial species, like Pseudoflavonifractor and Faecalibacterium were significantly increased only in old infected mice, correlating with increased intestinal inflammatory mRNA up-regulation from old mice tissue. Histologic analyses of gastric tissues showed extensive lesions in the Listeria-infected old mice, more so in the non-glandular region and fundus than in the pylorus. Commensal species like Lactobacillus, Clostridiales, and Akkermansia were only abundant in infected young-adult mice but their abundance diminished in the infected old mice. Listeriosis in old mice enhances the abundance of butyrate-producing inflammatory members of the Ruminococcaceae/Lachnospiraceae bacteria while reducing/eliminating beneficial commensals in the gut. Results of this study indicate that, aging may affect the composition of gut microbiota and increase the risk of invasive L. monocytogenes infection.

scholarly journals Long-term diet-induced obesity does not lead to learning and memory impairment in adult mice

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257921
Author(s):  
Judith Leyh ◽  
Karsten Winter ◽  
Madlen Reinicke ◽  
Uta Ceglarek ◽  
Ingo Bechmann ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Dietary Fat ◽  
General Health ◽  
Memory Impairment ◽  
Normal Diet ◽  
Morris Water Maze Test ◽  
Assessment Protocol ◽  
Adult Mice ◽  
Y Maze

Obesity arising from excessive dietary fat intake is a risk factor for cognitive decline, dementia and neurodegenerative diseases, including Alzheimer’s disease. Here, we studied the effect of long-term high-fat diet (HFD) (24 weeks) and return to normal diet (ND) on behavioral features, microglia and neurons in adult male C57BL/6J mice. Consequences of HFD-induced obesity and dietary changes on general health (coat appearance, presence of vibrissae), sensory and motor reflexes, learning and memory were assessed by applying a phenotypic assessment protocol, the Y maze and Morris Water Maze test. Neurons and microglia were histologically analyzed within the mediobasal hypothalamus, hippocampus and frontal motor cortex after long-term HFD and change of diet. Long periods of HFD caused general health issues (coat alterations, loss of vibrissae), but did not affect sensory and motor reflexes, emotional state, memory and learning. Long-term HFD increased the microglial response (increased Iba1 fluorescence intensity, percentage of Iba1-stained area and Iba1 gene expression) within the hypothalamus, but not in the cortex and hippocampus. In neither of these regions, neurodegeneration or intracellular lipid droplet accumulation was observed. The former alterations were reversible in mice whose diet was changed from HFD to ND. Taken together, long periods of excessive dietary fat alone do not cause learning deficits or spatial memory impairment, though HFD-induced obesity may have detrimental consequences for cognitive flexibility. Our data confirm the selective responsiveness of hypothalamic microglia to HFD.

Sign in / Sign up

Export Citation Format

Share Document