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1.
Food Funct ; 14(19): 8692-8710, 2023 Oct 02.
Article in English | MEDLINE | ID: mdl-37724008

ABSTRACT

The incidences of short-term or long-term adverse maternal and fetal outcomes caused by maternal diabetes are increasing. Due to toxicity or side effects, economic pressures, and other problems associated with injections or oral hypoglycemic drugs, many researchers have investigated natural treatment methods. Polyphenols can protect against chronic pathologies by regulating numerous physiological processes and provide many health benefits. Moreover, polyphenols have anti-diabetic properties and can be used to treat diabetic complications. Diets rich in polyphenols are beneficial to pregnant women with diabetes. Here, we review the epidemiological and experimental evidence on the impact of dietary polyphenols on maternal and fetal outcomes in pregnant women with diabetes, and the effects of polyphenols on biological changes and possible mechanisms. Previous data (mainly from in vitro and animal experiments) showed that polyphenols can alleviate gestational diabetes mellitus and diabetic embryopathy by reducing maternal hyperglycemia and insulin resistance, alleviating inflammation and oxidative stress, and regulating related signaling pathways. Although polyphenols have shown many health benefits, further research is needed to better understand the complex interactions between polyphenols and maternal diabetes.

2.
Mol Brain ; 13(1): 162, 2020 11 23.
Article in English | MEDLINE | ID: mdl-33228716

ABSTRACT

Sirtuin 1 (SIRT1), is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase and a candidate gene for depression. Nicotinamide (NAM), a form of vitamin B3, is reported as a potential inhibitor of SIRT1. Our previous study found that the 24-h-restraint stress could induce long-term depressive-like phenotypes in mice. These mice displayed increased SIRT1 activity. Here, we studied whether NAM was capable of attenuating depressive behaviors through inhibiting SIRT1 activity. Surprisingly, the application of NAM significantly reversed the depressive behaviors but increased SIRT1 activity further. In contrast, the level of adenosine triphosphate (ATP) was reduced in the restraint model for depression, and recovered by the administration of NAM. Furthermore, the Sirt1flox/flox; Nestin-Cre mice exhibited antidepressant behaviors and increased ATP levels. These data suggest that ATP plays an important role in depression pathogenesis, and NAM could be a potential treatment method for depression by regulating ATP independent of SIRT1 activity.


Subject(s)
Behavior, Animal , Depression/drug therapy , Depression/metabolism , Niacinamide/therapeutic use , Sirtuin 1/metabolism , Adenosine Triphosphate/metabolism , Animals , Antidepressive Agents/pharmacology , Antidepressive Agents/therapeutic use , Behavior, Animal/drug effects , Integrases/metabolism , Male , Mice, Inbred C57BL , Mice, Knockout , Nestin/metabolism , Niacinamide/pharmacology
3.
Mol Brain ; 12(1): 91, 2019 11 07.
Article in English | MEDLINE | ID: mdl-31699123

ABSTRACT

Autism spectrum disorder (ASD) is a heterogeneous group of complex neurodevelopmental disorders without a unique or definite underlying pathogenesis. Although savant syndrome is common in ASD, few models are available for studying the molecular and cellular mechanisms of this syndrome. In this study, we generated urinary induced pluripotent stem cells (UiPSCs) from a 13-year-old male autistic savant with exceptional memory. The UiPSC-derived neurons of the autistic savant exhibited upregulated expression levels of ASD genes/learning difficulty-related genes, namely PAX6, TBR1 and FOXP2, accompanied by hypertrophic neural somas, enlarged spines, reduced spine density, and an increased frequency of spontaneous excitatory postsynaptic currents. Although this study involved only a single patient and a single control because of the rarity of such cases, it provides the first autistic savant UiPSC model that elucidates the potential cellular mechanisms underlying the condition.


Subject(s)
Autistic Disorder/pathology , Autistic Disorder/physiopathology , Memory , Neurons/pathology , Adolescent , Animals , Autistic Disorder/genetics , Autistic Disorder/urine , Cell Differentiation , Child , Dendritic Spines/metabolism , Excitatory Postsynaptic Potentials , Humans , Hypertrophy , Induced Pluripotent Stem Cells/metabolism , Male , Mice, Inbred ICR , Models, Biological , Syndrome , Up-Regulation/genetics
4.
J Phys Condens Matter ; 31(38): 385403, 2019 Sep 25.
Article in English | MEDLINE | ID: mdl-31195373

ABSTRACT

We propose a general framework to classify the topological edge modes in two dimensional topological crystalline superconductors with time-reversal symmetry, which are protected by different crystalline symmetries. The realization of topological crystalline phases is investigated in the superconductors and a criterion for distinguishing topological phases in crystalline superconductor both with mirror and mirror-inversion symmetry is founded. In these topological phases, Majorana edge modes can be identified along the mirror invariant line, while topological edge modes in the AIII class exist along the mirror-inversion invariant line. Furthermore, for the time-reversal invariant superconductor when only the mirror-inversion symmetry is preserving, topological edge modes in the AIII class with nearly flat band emerge in the mirror-inversion parity subspace.

5.
J Phys Condens Matter ; 31(12): 125402, 2019 Mar 27.
Article in English | MEDLINE | ID: mdl-30650403

ABSTRACT

We propose a model of two-leg ladder topological insulator in which the spin-orbit couplings are presented in both intra-chain and inter-chain interactions. The topological phase supports four fractional charged edge states localized at opposite ends of the ladder, which belongs to the chiral symplectic (CII) class protected by time-reversal symmetry and chiral symmetry. In our model, the presence of time-reversal and chiral symmetry generates fourfold degeneracy for the edge states, and the two edge states with same chirality at one end of the ladder each carries half charge. In contrast to the two edge states spatially localized at one end of the ladder being not distinguished, these two edge states can be detected by the momentum density. The experimental scheme for realizing our model with cold atoms in optical lattice is discussed. By introducing a magnetic field in the x direction, the system is driven from CII class to AIII class. In AIII class, there exist two distinct topological phases that exhibit four degenerate edge states and two degenerate edge states in the gap, respectively. As same as the system in CII class, each edge state carries a half charge in AIII class.

6.
Neuropharmacology ; 131: 364-376, 2018 03 15.
Article in English | MEDLINE | ID: mdl-29329879

ABSTRACT

Increasing evidence has suggested that depression is a neuropsychiatric condition associated with neuroplasticity within specific brain regions. However, the mechanisms by which neuroplasticity exerts its effects in depression remain largely uncharacterized. In the present study we show that chronic stress effectively induces depression-like behaviors in rats, an effect which was associated with structural changes in dendritic spines and synapse abnormalities within neurons of the ventromedial prefrontal cortex (vmPFC). Moreover, unpredictable chronic mild stress (UCMS) exposure significantly increased the expression of miR-134 within the vmPFC, an effect which was paralleled with a decrease in the levels of expression and phosphorylation of the synapse-associated proteins, LIM-domain kinase 1 (Limk1) and cofilin. An intracerebral infusion of the adenovirus associated virus (AAV)-miR-134-sponge into the vmPFC of stressed rats, which blocks mir-134 function, significantly ameliorated neuronal structural abnormalities, biochemical changes and depression-like behaviors. Chronic administration of ginsenoside Rg1 (40 mg/kg, 5 weeks), a potential neuroprotective agent extracted from ginseng, significantly ameliorated the behavioral and biochemical changes induced by UCMS exposure. These results suggest that miR-134-mediated dysregulation of structural plasticity may be related to the display of depression-like behaviors in stressed rats. The neuroprotective effects of ginsenoside Rg1, which produces an antidepressant like effect in this model of depression, appears to result from modulation of the miR-134 signaling pathway within the vmPFC.


Subject(s)
Antidepressive Agents/pharmacology , Depressive Disorder/metabolism , Ginsenosides/pharmacology , Lim Kinases/metabolism , MicroRNAs/metabolism , Neuronal Plasticity/physiology , Actin Depolymerizing Factors/metabolism , Animals , Dendritic Spines/drug effects , Dendritic Spines/metabolism , Dendritic Spines/pathology , Depressive Disorder/drug therapy , Depressive Disorder/pathology , Disease Models, Animal , Down-Regulation/drug effects , Male , MicroRNAs/antagonists & inhibitors , Neuronal Plasticity/drug effects , Prefrontal Cortex/drug effects , Prefrontal Cortex/metabolism , Prefrontal Cortex/pathology , Random Allocation , Rats, Wistar , Signal Transduction/drug effects , Stress, Psychological/drug therapy , Stress, Psychological/metabolism , Synapses/drug effects , Synapses/metabolism , Synapses/pathology
7.
Eur J Neurosci ; 44(2): 1878-85, 2016 07.
Article in English | MEDLINE | ID: mdl-27062560

ABSTRACT

Depression is a major neuropsychiatric disorder that exerts deleterious effects upon public health. However, the neuronal mechanisms of depression remain largely uncharacterized, which has retarded the identification and development of effective therapeutic tools for the treatment of this disorder. The aim of this study was to explore the neuronal mechanisms underlying the protective effects of ginsenoside Rg1, a natural steroidal saponin found in ginseng, against chronic stress-induced depression.The results showed that chronic administration of ginsenoside Rg1 (40 mg/kg, i.p., 5 weeks) significantly ameliorated depression-like behaviours in rats as assessed in the sucrose preference and forced swim tests. Furthermore, chronic stress decreased the phosphorylation levels of the extracellular signal-regulated kinase and cAMP-response element-binding protein in the prefrontal cortex as well as producing a reduction of brain-derived neurotrophic factor expression. Of particular importance, all reductions in these parameters were significantly reversed by pre-treatment with ginsenoside Rg1. Taken together, the results of the present study suggest that the antidepressant-like effect of ginsenoside Rg1 might be mediated, at least in part, by activating the cAMP-response element-binding protein-brain-derived neurotrophic factor system within the prefrontal cortex. These findings not only reveal some of the underlying neuronal mechanisms of depression, but also the therapeutic potential of ginsenoside Rg1 as a preventive agent in the treatment of depression.


Subject(s)
Brain-Derived Neurotrophic Factor/metabolism , Central Nervous System Agents/pharmacology , Depression/drug therapy , Ginsenosides/pharmacology , Prefrontal Cortex/drug effects , Stress, Psychological/drug therapy , Animals , Brain-Derived Neurotrophic Factor/genetics , Central Nervous System Agents/administration & dosage , Central Nervous System Agents/therapeutic use , Cyclic AMP Response Element-Binding Protein/metabolism , Depression/etiology , Extracellular Signal-Regulated MAP Kinases/metabolism , Ginsenosides/administration & dosage , Ginsenosides/therapeutic use , Male , Prefrontal Cortex/metabolism , Prefrontal Cortex/physiology , Rats , Rats, Wistar , Stress, Psychological/complications
8.
Clin Exp Pharmacol Physiol ; 43(5): 562-8, 2016 May.
Article in English | MEDLINE | ID: mdl-26901099

ABSTRACT

Hydrogen sulphide (H2 S) is generated endogenously from L-cysteine (L-Cys) by the enzymes cystathionine-ß-synthase (CBS) and cystathionine-γ-lyase (CSE). In addition, L-Cys is commonly used as a precursor in the food and pharmaceutical industries. The aim of the present study is to determine whether L-Cys regulates intestinal nutrient transport. To that end, the presence of CBS and CSE in the jejunum epithelium was assessed by immunohistochemistry, Western blotting and the methylene blue assay. In addition, in vivo L-Cys (100 mg/kg, administered immediately after the glucose load) significantly increased blood glucose levels 30 min after the oral administration of glucose to mice. This effect of L-Cys was completely blocked by amino-oxyacetic acid (AOA; 50 mg/kg; administered at the same time as L-Cys) an inhibitor of CBS. Measurements of the short-circuit current (Isc) in the rat jejunum epithelium revealed that L-Cys (1 mmol/L; 6 min before the administration of L-alanine) enhances Na(+)-coupled L-alanine or glucose transport, and that this effect is inhibited by AOA (1 mmol/L;10 min before the administration of L-Cys), but not D,L-propargylglycine (PAG;1 mmol/L; 10 min before the administration of L-Cys), a CSE inhibitor. Notably, L-Cys-evoked enhancement of nutrient transport was alleviated by glibenclamide (Gli;0.1 mmol/L; 10 min before the administration of L-Cys), a K(+) channel blocker. Together, the data indicate that L-Cys enhances jejunal nutrient transport, suggesting a new approach to future treatment of nutrition-related maladies, including a range of serious health consequences linked to undernutrition.


Subject(s)
Cystathionine beta-Synthase/metabolism , Cysteine/pharmacology , Hydrogen Sulfide/metabolism , Intestinal Absorption/drug effects , Jejunum/drug effects , Jejunum/metabolism , Signal Transduction/drug effects , Animals , Blood Glucose/metabolism , Intestinal Mucosa/cytology , Intestinal Mucosa/drug effects , Intestinal Mucosa/metabolism , Jejunum/cytology , Male , Mice , Postprandial Period/drug effects , Rats
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