scholarly journals Capsosiphon fulvescens Glycoproteins Enhance Probiotics-Induced Cognitive Improvement in Aged Rats

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 837 ◽  
Author(s):  
Jeong Hwan Oh ◽  
Taek-Jeong Nam ◽  
Youn Hee Choi
Keyword(s):  
Dorsal Hippocampus ◽  
Synergistic Effects ◽  
Elongation Factor ◽  
Underlying Mechanism ◽  
Related Factor ◽  
Aged Rats ◽  
Bdnf Expression ◽  
Cognitive Improvement ◽  
Capsosiphon Fulvescens ◽  
Eef2 Kinase

Aging-induced cognitive dysfunction can be regulated by probiotics through bidirectional communication with the brain. This study aimed to investigate whether Capsosiphon fulvescens glycoproteins (Cf-hGP) enhanced probiotic-induced improvement of memory in aged rats and the underlying mechanism in the dorsal hippocampus. Cf-hGP were isolated using lectin resin. Cf-hGP (15 mg/kg/day) and/or Lactobacillus plantarum (L. plantarum) (109 CFU/rat/day) were orally administered once a day for 4 weeks. Co-treatment with Cf-hGP and L. plantarum synergistically improved spatial memory in aged rats, which was overturned by functional blocks of brain-derived neurotrophic factor (BDNF) signaling. Increases in BDNF expression and nuclear factor erythroid 2-related factor 2 (Nrf2) phosphorylation were accompanied by mono- and/or co-administration in the dorsal hippocampus, while c-Jun N-terminal kinase (JNK) phosphorylation and glucose-regulated protein 78 expression were decreased. These synergistic effects were downregulated by blocks of BDNF/Nrf2-mediated signaling. In particular, co-treatment, not mono-treatment, reduced phosphorylation of eukaryotic elongation factor 2 (eEF2) regulated by eEF2 kinase and protein phosphatase 2A. Additionally, co-treatment downregulated the interaction between eEF2 kinase and JNK. These data demonstrated that cognitive impairment in aged rats was synergistically diminished by co-treatment with Cf-hGP and L. plantarum through BDNF-mediated regulation of Nrf2 and eEF2 signaling pathways in the dorsal hippocampus.

scholarly journals Variations in Antioxidant Genes and Male Infertility

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Bolan Yu ◽  
Zhaofeng Huang
Keyword(s):  
Male Infertility ◽  
Population Studies ◽  
Sperm Quality ◽  
Synergistic Effects ◽  
Related Factor ◽  
Antioxidant Genes ◽  
Functional Polymorphisms ◽  
Normal Sperm ◽  
Oxide Synthase ◽  
Defective Spermatogenesis

Oxidative stress and reactive oxygen species (ROS) are generated from both endogenous and environmental resources, which in turn may cause defective spermatogenesis and male infertility. Antioxidant genes, which include catalase (CAT), glutathione peroxidase (GPX), glutathioneS-transferase (GST), nitric oxide synthase (NOS), nuclear factor erythroid 2-related factor 2 (NRF2), and superoxide dismutase (SOD), play important roles in spermatogenesis and normal sperm function. In this review, we discuss the association between variations in major antioxidant genes and male infertility. Numerous studies have suggested that genetic disruption or functional polymorphisms in these antioxidant genes are associated with a higher risk for male infertility, which include low sperm quality, oligoasthenoteratozoospermia, oligozoospermia, and subfertility. The synergistic effects of environmental ROS and functional polymorphisms on antioxidant genes that result in male infertility have also been reported. Therefore, variants in antioxidant genes, which independently or synergistically occur with environmental ROS, affect spermatogenesis and contribute to the occurrence of male infertility. Large cohort and multiple center-based population studies to identify new antioxidant genetic variants that increase susceptibility to male infertility as well as validate its potential as genetic markers for diagnosis and risk assessment for male infertility for precise clinical approaches are warranted.

Conifer Essential Oils Reversed Amyloid Beta1-42 Action by Modulating BDNF and ARC Expression in The Rat Hippocampus

2021 ◽  
Vol 20 ◽  
Author(s):  
Paula Alexandra Postu ◽  
Adrian Tiron ◽  
Crina Elena Tiron ◽  
Dragoș Lucian Gorgan ◽  
Marius Mihasan ◽  
...  
Keyword(s):  
Essential Oils ◽  
Dna Fragmentation ◽  
Rat Model ◽  
Pinus Halepensis ◽  
Chemical Constituents ◽  
Gene Expressions ◽  
Bdnf Expression ◽  
Neuroprotective Effects ◽  
Positive Effects ◽  
Cognitive Improvement

Background: The conifer species Pinus halepensis (Pinaceae) and Tetraclinis articulata (Cupressaceae) are widely used in traditional medicine due to their health beneficial properties. Objective: This study aimed to investigate the mechanisms by which P. halepensis and T. articulata essential oils (1% and 3%) could exhibit neuroprotective effects in an Alzheimer's disease (AD) rat model, induced by intracerebroventricular (i.c.v.) administration of amyloid beta1-42 (Aβ1-42). Method: The essential oils were administered by inhalation to the AD rat model, once daily, for 21 days. DNA fragmentation was assessed through Cell Death Detection ELISA kit. Brain-derived neurotrophic factor (BDNF), activity-regulated cytoskeleton-associated protein (ARC) and interleukin-1β (IL-1β) gene expressions were determined by RT-qPCR analysis, while BDNF and ARC protein expressions were assessed using immunohistochemistry technique. Results: Our data showed that both essential oils substantially attenuated memory impairments, with P. halepensis mainly stimulating ARC expression and T. articulata mostly enhancing BDNF expression. Also, the inhalation of essential oils reduced IL-1β expression and induced positive effects against DNA fragmentation associated with Aβ1-42-induced toxicity, further contributing to the cognitive improvement in the rats with AD-like model. Conclusion: Our findings provide further evidence that these essential oils and their chemical constituents could be natural agents of therapeutic interest against Aβ1-42-induced neurotoxicity.

Functional Characterization of Des-IGF-1 Action at Excitatory Synapses in the CA1 Region of Rat Hippocampus

2005 ◽  
Vol 94 (1) ◽  
pp. 247-254 ◽  
Author(s):  
Melinda M. Ramsey ◽  
Michelle M. Adams ◽  
Olusegun J. Ariwodola ◽  
William E. Sonntag ◽  
Jeff L. Weiner
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Functional Characterization ◽  
Excitatory Postsynaptic Potential ◽  
Excitatory Synapses ◽  
Aged Rats ◽  
Cognitive Improvement ◽  
Ca1 Region

Insulin-like growth factor-1 (IGF-1) and growth hormone play a major role in the growth and development of tissues throughout the mammalian body. Plasma IGF-1 concentrations peak during puberty and decline with age. We have determined that chronic treatments to restore plasma IGF-1 concentrations to adult levels attenuate spatial learning deficits in aged rats, but little is known of the acute actions of IGF-1 in the brain. To this end, we utilized hippocampal slices from young Sprague-Dawley rats to characterize the acute effects of des-IGF-1 on excitatory synaptic transmission in the CA1 region. We observed a 40% increase in field excitatory postsynaptic potential (fEPSP) slope with application of des-IGF-1 (40 ng/ml) and used whole cell patch-clamp recordings to determine that this enhancement was due to a postsynaptic mechanism involving α-amino-3-hydroxyl-5-methyl-4-isoxazolepropionate (AMPA) but not N-methyl-d-aspartate receptors. Furthermore, the enhancement was completely blocked by the broad-spectrum tyrosine kinase inhibitor, genistein (220 μM), and significantly reduced by the PI3K blockers wortmannin (1 μM) and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (10 μM), suggesting that the effect was predominantly dependent on PI3K activation. This characterization of the acute actions of des-IGF-1 at hippocampal excitatory synapses may provide insight into the mechanism by which long-term increases in plasma IGF-1 impart cognitive benefits in aged rats. Increases in AMPA receptor-mediated synaptic transmission may contribute directly to cognitive improvement or initiate long-term changes in synthesis of proteins such as brain-derived neurotrophic factor that are important to learning and memory.

A Theoretical Perspective of the Structure and Thermodynamics of Secondary Organic Aerosols from Toluene: Molecular Hierarchical Synergistic Effects

2022 ◽  
Author(s):  
Xianli Duan ◽  
Xianyu Song ◽  
Shi Ruifang ◽  
Wang Xuan ◽  
Suhang Chen ◽  
...  
Keyword(s):  
Liquid Fuel ◽  
Secondary Organic Aerosols ◽  
Secondary Organic Aerosol ◽  
Synergistic Effects ◽  
Theoretical Perspective ◽  
Organic Aerosols ◽  
Organic Aerosol ◽  
Underlying Mechanism ◽  
Important Constituent

Toluene is an important constituent of liquid fuel, and it contributes to the formation of secondary organic aerosol (SOA) under photochemical conditions. However, the underlying mechanism of toluene SOA is...

scholarly journals A Novel mTOR-Regulated Phosphorylation Site in Elongation Factor 2 Kinase Modulates the Activity of the Kinase and Its Binding to Calmodulin

2004 ◽  
Vol 24 (7) ◽  
pp. 2986-2997 ◽  
Author(s):  
Gareth J. Browne ◽  
Christopher G. Proud
Keyword(s):  
Amino Acids ◽  
Protein Kinase ◽  
Phosphorylation Site ◽  
Elongation Factor ◽  
Mtor Pathway ◽  
Mtor Signaling ◽  
Chain Elongation ◽  
Binding Motif ◽  
Elongation Factor 2 ◽  
Eef2 Kinase

ABSTRACT Eukaryotic elongation factor 2 (eEF2) kinase is an unusual calcium- and calmodulin-dependent protein kinase that is regulated by insulin through the rapamycin-sensitive mTOR pathway. Here we show that insulin decreases the ability of eEF2 kinase to bind calmodulin in a rapamycin-sensitive manner. We identify a novel phosphorylation site in eEF2 kinase (Ser78) that is located immediately next to its calmodulin-binding motif. Phosphorylation of this site is increased by insulin in a rapamycin-sensitive fashion. Regulation of the phosphorylation of Ser78 also requires amino acids and the protein kinase phosphoinositide-dependent kinase 1. Mutation of this site to alanine strongly attenuates the effects of insulin and rapamycin both on the binding of calmodulin to eEF2 kinase and on eEF2 kinase activity. Phosphorylation of Ser78 is thus likely to link insulin and mTOR signaling to the control of eEF2 phosphorylation and chain elongation. This site is not a target for known kinases in the mTOR pathway, e.g., the S6 kinases, implying that it is phosphorylated by a novel mTOR-linked protein kinase that serves to couple hormones and amino acids to the control of translation elongation. eEF2 kinase is thus a target for mTOR signaling independently of previously known downstream components of the pathway.

The dilemma of social commerce

2020 ◽  
Vol 30 (3) ◽  
pp. 1059-1080 ◽  
Author(s):  
Xiaodong Li ◽  
Chuang Wang ◽  
Yanping Zhang
Keyword(s):  
Avoidance Behavior ◽  
Information Overload ◽  
Negative Relationship ◽  
Underlying Mechanism ◽  
Tie Strength ◽  
Related Factor ◽  
Social Commerce ◽  
Content Type ◽  
Positive Effects ◽  
Shared Language

PurposeDue to customers' extensive avoidance behavior, social commerce may be less successful than anticipated. This study investigates the underlying mechanism and antecedents that influence customers' avoidance of peer-generated advertisements.Design/methodology/approachBased on the general framework of avoidance behavior, we propose a theoretical model for the context of a mobile social network, with tie strength as the user-related factor and violation of shared language, advertisement relevance and information overload as contextual variables. Using survey data collected from 334 customers on WeChat, we empirically examine the research model and hypotheses.FindingsTie strength and advertisement relevance are negatively associated with avoidance behavior, whereas information overload and violation of shared language have significantly positive effects. Furthermore, tie strength weakens the negative relationship between violation of shared language and avoidance behavior but strengthens the positive relationship between advertisement relevance and avoidance behavior.Originality/valueThe findings extend understanding of advertisement avoidance behavior and can guide practitioners' improvement of advertising efficiency in mobile social networks.

scholarly journals Resistance exercise-induced S6K1 kinase activity is not inhibited in human skeletal muscle despite prior activation of AMPK by high-intensity interval cycling

2015 ◽  
Vol 308 (6) ◽  
pp. E470-E481 ◽  
Author(s):  
William Apró ◽  
Marcus Moberg ◽  
D. Lee Hamilton ◽  
Björn Ekblom ◽  
Gerrit van Hall ◽  
...  
Keyword(s):  
Resistance Exercise ◽  
Kinase Activity ◽  
Vastus Lateralis ◽  
Elongation Factor ◽  
Underlying Mechanism ◽  
Hypertrophic Response ◽  
Gene And Protein Expression ◽  
Mtorc1 Signaling ◽  
Ampk Activity ◽  
Interval Cycling

Combining endurance and strength training in the same session has been reported to reduce the anabolic response to the latter form of exercise. The underlying mechanism, based primarily on results from rodent muscle, is proposed to involve AMPK-dependent inhibition of mTORC1 signaling. This hypothesis was tested in eight trained male subjects who in randomized order performed either resistance exercise only (R) or interval cycling followed by resistance exercise (ER). Biopsies taken from the vastus lateralis before and after endurance exercise and repeatedly after resistance exercise were assessed for glycogen content, kinase activity, protein phosphorylation, and gene expression. Mixed muscle fractional synthetic rate was measured at rest and during 3 h of recovery using the stable isotope technique. In ER, AMPK activity was elevated immediately after both endurance and resistance exercise (∼90%, P < 0.05) but was unchanged in R. Thr389 phosphorylation of S6K1 was increased severalfold immediately after exercise ( P < 0.05) in both trials and increased further throughout recovery. After 90 and 180 min recovery, S6K1 activity was elevated (∼55 and ∼110%, respectively, P < 0.05) and eukaryotic elongation factor 2 phosphorylation was reduced (∼55%, P < 0.05) with no difference between trials. In contrast, markers for protein catabolism were differently influenced by the two modes of exercise; ER induced a significant increase in gene and protein expression of MuRF1 ( P < 0.05), which was not observed following R exercise only. In conclusion, cycling-induced elevation in AMPK activity does not inhibit mTOR complex 1 signaling after subsequent resistance exercise but may instead interfere with the hypertrophic response by influencing key components in protein breakdown.

scholarly journals Aging-dependent downregulation of SUV39H1 histone methyltransferase increases susceptibility to stress-induced depressive behavior

2021 ◽  
Author(s):  
Jung-Eun Lee ◽  
So-Young Park ◽  
Pyung-Lim Han
Keyword(s):  
Chromatin Immunoprecipitation ◽  
Underlying Mechanism ◽  
Histone Methyltransferase ◽  
Bdnf Expression ◽  
Ht22 Cells ◽  
Depressive Behavior ◽  
Aged Mice ◽  
Gene Expression Alteration ◽  
Induced Changes ◽  
The Brain

Abstract Aging induces cellular and molecular changes including gene expression alteration in the brain, which might be associated with aging-dependent increase in vulnerability to stress-induced depression. However, the underlying mechanism is not clearly understood. In the present study, we investigate how aging changes the ability to cope with stress and increases sensitivity to stress. Aged mice have decreased expression of SUV39H1 histone methyltransferase and increased expression of Mkp-1 in the hippocampus. The siRNA-mediated knockdown of SUV39H1 increases Mkp-1 expression and suppresses p-CREB and Bdnf expression in HT22 cells and in the hippocampus of mice. Chromatin immunoprecipitation assays indicate that the levels of SUV39H1 and methylated histone-H3 bound to the promoter of the Mkp-1 in the hippocampus are reduced in aged mice. Aged mice exhibit depression-like behavior following weak stress that does not induce depressive behavior in young mice. Rosmarinic acid, a phenolic compound that increases SUV39H1 expression, reverses stress-induced changes of SUV39H1, Mkp-1, and Bdnf expression in the hippocampus via an overlapping but distinct mechanism from those of fluoxetine and imipramine and produces anti-depressive effects. These results suggest that aging increases susceptibility to stress via downregulation of SUV39H1 and changes in SUV39H1-regulated signaling pathways in the hippocampus.

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