Ubiquitinome Analysis Uncovers Alterations in Synaptic Proteins and Glucose Metabolism Enzymes in the Hippocampi of Adolescent Mice Following Cold Exposure.

Cold exposure exerts negative effects on hippocampal nerve development in adolescent mice, but the underlying mechanisms are not fully understood. Given that ubiquitination is essential for neurodevelopmental processes, we attempted to investigate the effects of cold exposure on the hippocampus from the perspective of ubiquitination. By conducting a ubiquitinome analysis, we found that cold exposure caused changes in the ubiquitination levels of a variety of synaptic-associated proteins.

Integrated metabolism and epigenetic modifications in the macrophages of mice in responses to cold stress.

The negative effects of low temperature can readily induce a variety of diseases. We sought to understand the reasons why cold stress induces disease by studying the mechanisms of fine-tuning in macrophages following cold exposure. We found that cold stress triggers increased macrophage activation accompanied by metabolic reprogramming of aerobic glycolysis.

Procyanidin B2 alleviates liver injury caused by cold stimulation through Sonic hedgehog signalling and autophagy.

Procyanidin B2 (PB2), a naturally occurring flavonoid abundant in a wide range of fruits, has been shown to exert antioxidant, anti-inflammatory and anticancer properties. However, the role of PB2 in the prevention of cold stimulation (CS)-induced liver injury. The present study was undertaken to determine the effects of PB2 on liver injury induced by cold stimulation and its potential molecular mechanisms.

O-GlcNAc / Akt pathway regulates glucose metabolism and reduces apoptosis in liver of piglets with acute cold stress.

Cold stress is one of the serious factors restricting the development of animal husbandry in cold areas. Cold exposure can easily lead to cold stress, slow growth and even death of newborn animals. O-GlcNAcylation modification can act as type of "stress receptor" and"nutrition sensor" in a variety of stress responses, however, it is not clear how O-GlcNAcylation can regulate glucose metabolism in the liver of piglets under cold stress.

GABA-mediated activated microglia induce neuroinflammation in the hippocampus of mice following cold exposure through the NLRP3 inflammasome and NF-κB signaling pathways.

Chronic cold stress has long-term dramatic effects on the animal immune and neuroendocrine systems. As one of the important regions of the brain, the hippocampus is the main region involved in response to stressors. Nevertheless, the impact to the hippocampus following cold exposure and the underlying mechanism involved are not clear.

ActivinA activates Notch1-Shh signaling to regulate proliferation in C2C12 skeletal muscle cells.

The myoblast is a precursor cell that rebuilds muscle tissue after trauma in human and animal skeletal muscle tissue. Proliferation of myoblasts is important for skeletal muscle damage repair and is controlled by numerous transcription factors and signals. The regulation of these signaling pathways and their complex interactions are not fully understood.

[Effects of α-enolase gene interference expression on proliferation and apoptosis of follicular granulosa cells from Zi geese].

To study the effects of α-enolase () gene interference expression on proliferation, and cell cycle of follicular granulosa cells from Zi geese. F1 follicular granulosa cells were primary cultured (mixed culture), which were divided into four groups: interference expression group (RNAi), unrelated sequence group (NC), culture group (Control), transfection reagent group (Lip). The apoptosis rate and cell cycle phase of the interference group and the control group were detected by the flow cytometry.

Effects of α-enolase Gene Silencing on Reproductive-related Hormone Receptor Expression and Steroid Hormone Synthesis of Primary Granulosa Cells from Goose F1 Follicles.

Introduction: Enolases are enzymes in the glycolytic pathway, which catalyse the reversible conversion of D-2-phosphoglycerate into phosphoenol pyruvate in the second half of the pathway. In this research, the effects of α-enolase () on steroid reproductive-related hormone receptor expression and on hormone synthesis of primary granulosa cells from goose F1 follicles were studied.

Material And Methods: Primary granulosa cells from the F1 follicles of eight healthy 8-month-old Zi geese were separated and cultured.

Down-regulation of miR-383-5p suppresses apoptosis in oxidative stress rat hepatocytes by targeting Bcl2.

miRNAs are a class of small non-coding RNAs that are involved in various biological processes. In the preliminary work of the laboratory, found that miR-383-5p was down-regulated in the liver tissue of acute cold stress rats and has been shown to be an important regulatory factor in tumour proliferation, but there are very few studies involving the mediation of cold stress in rat liver tissues. Therefore, the purpose of this study was to determine the effect of miR-383-5p on the livers of cold stress rats by simulating the cold stress state of rat liver tissues in vitro using H O to induce rat hepatocyte oxidative stress.

Effects of prenatal cold stress on maternal serum metabolomics in rats.

Our previous studies have shown that prenatal cold stress leads to placental inflammatory response and induces anxiety-like behavior reduced in offspring rats. However, the role and mechanisms by which prenatal cold stress affects offspring remain unclear. The aim of this study was to determine the metabolic profiles from the maternal serum and helpful in understanding the role and mechanisms by which prenatal cold stress affects the offspring.

Identification, functional prediction, and key lncRNA verification of cold stress-related lncRNAs in rats liver.

Cold stimulation reduces the quality of animal products and increases animal mortality, causing huge losses to the livestock industry in cold regions. Long non-coding RNAs (lncRNAs) take part in many biological processes through transcriptional regulation, intracellular material transport, and chromosome remodeling. Although cold stress-related lncRNAs have been reported in plants, no research is available on the characteristic and functional analysis of lncRNAs after cold stress in rats.

Metabonomics analysis of Zi goose follicular granulosa cells using ENO1 gene expression interference.

The Zi goose is native to North-east China and is noted for its high egg production. Alpha enolase (ENO1) is a glycolytic enzyme which functions as a plasminogen receptor in follicular granulosa cells (FGCs), with several studies showing that FGCs can support follicular development. By transfecting the ENO1 interfering plasmid (shRNA) into FGCs, ENO1 expression in these cells was downregulated, suggesting the successful knock-down of ENO1 in these cells.

Oxidation Stress-Mediated MAPK Signaling Pathway Activation Induces Neuronal Loss in the CA1 and CA3 Regions of the Hippocampus of Mice Following Chronic Cold Exposure.

Chronic stress can damage homeostasis and induce various primary diseases. Although chronic cold stress is becoming an increasing problem for people who must work or live in extreme environments, risk-induced diseases in the central nervous system remain unstudied. Male C57BL/6 mice were exposed to an environment of 4 °C, 3 h per day for 1, 2, and 3 weeks and homeostasis in the hippocampus and neuronal apoptosis were evaluated by Western blotting, immunohistochemistry, TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, and immunofluorescence.

Neuroinflammation induced by secretion of acetylated HMGB1 from activated microglia in hippocampi of mice following chronic cold exposure.

Stress is a nonspecific response to adverse circumstances and chronic stress can destroy homeostasis, leading to various primary diseases. Although chronic cold stress is becoming increasingly important for individuals living or working in extreme environments, the risk of associated disorders of the central nervous system remains unstudied. Here, male C57BL/6 mice were exposed to a temperature of 4 °C, for three hours each day for one, two or three weeks.

Corticosterone Excess-Mediated Mitochondrial Damage Induces Hippocampal Neuronal Autophagy in Mice Following Cold Exposure.

Cold stress can induce autophagy mediated by excess corticosterone (CORT) in the hippocampus, but the internal mechanism induced by cold stress is not clear. In vivo, male and female C57BL/6 mice were stimulated in 4 °C, 3 h per day for 1 week to build the model of cold sress. In vitro, hippocampal neuronal cell line (HT22) cells were incubated with or without mifepristone (RU486) for 1 h, then treated with 400 μM cortisol (CORT) for 3 h.

Microglia Activated by Excess Cortisol Induce HMGB1 Acetylation and Neuroinflammation in the Hippocampal DG Region of Mice Following Cold Exposure.

Cold stress can induce neuroinflammation in the hippocampal dentate gyrus (DG), but the mechanism underlying neuronal apoptosis induced by cold stress is not well-understood. To address this issue, male and female C57BL/6 mice were exposed to a temperature of 4 °C for 3 h per day for 1 week, and glial cell activation, neuronal apoptosis, and neuroinflammation were evaluated by western blotting, immunofluorescence, terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate (dUTP) nick end labeling, Nissl staining, and immunohistochemistry. Additionally, BV2 cells were treated with different concentrations of cortisol (CORT) for 3 h to mimic stress and molecular changes were assessed by western blotting, immunofluorescence, and co-immunoprecipitation.

Response of the maternal hypothalamus to cold stress during late pregnancy in rats.

Maternal stress is a key risk factor in the development of offspring. We previously identified prenatal cold stress-induced anxiety-like behavior reduced in the offspring of rats along with negative feedback regulation from the maternal hippocampus on the hypothalamic-pituitary-adrenal (HPA) axis during prenatal cold stress. However, the precise function of the maternal hypothalamus response to cold stress during late pregnancy in rats has not yet been determined.

Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure.

Cold stress can induce neuronal apoptosis in the hippocampus, but the internal mechanism involving neuronal loss induced by cold stress is not clear. In vivo, male and female C57BL/6 mice were exposed to 4 °C, 3 h per day for 1 week. In vitro, HT22 cells were treated with different concentrations of cortisol (CORT) for 3 h.

Rno-miR-425-5p targets the DLST and SLC16A1 genes to reduce liver damage caused by excessive energy mobilization under cold stress.

MicroRNAs (miRNAs) are a class of single-stranded non-coding small RNA molecules, which participate in the regulation of many physiological processes, and play a crucial role in cancer, metabolism and other processes. Rno-miR-425-5p has been shown to play a role in the response to cold stress. To explore the mechanism by which rno-miR-425-5p regulates the response to cold stress, we analysed the candidate target genes of rno-miR-425-5p.

Effects of Cold-inducible RNA-binding Protein (CIRP) on Liver Glycolysis during Acute Cold Exposure in C57BL/6 Mice.

Cold-inducible RNA-binding protein (CIRP) is a stress-responsive protein involved in several signal transduction pathways required for cellular function, which are associated with apoptosis and proliferation. The present study aimed to investigate the possible effects of CIRP-mediated regulation of glucose metabolism in the liver following acute cold exposure. The livers and serum of male C57BL/6 mice were collected following cold exposure at 4 °C for 0 h, 2 h, 4 h, and 6 h.

Regulating glycolysis, the TLR4 signal pathway and expression of RBM3 in mouse liver in response to acute cold exposure.

At low temperatures, the liver increases glucose utilization and expresses RNA-binding motif 3 (RBM3) to cope with cold exposure. In this study, the expression of heat shock protein 70 (HSP70), Toll-like receptor 4 (TLR4), bone marrow differentiation factor 88 (MYD88), and phosphorylated nuclear factor-κB (NF-κB) was consistent with fluctuations in insulin in fasted cold-exposed mice. We also found up-regulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) in acute cold exposure with a decrease in core body temperature.

Activation of the MAPK signaling pathway induces upregulation of pro-apoptotic proteins in the hippocampi of cold stressed adolescent mice.

Stress induces many non-specific responses in the hippocampus, especially during adolescence. Low environmental temperature is known to induce stress, but its influence on the hippocampus, especially in adolescent mice is not clear. We compared apoptotic-related protein levels and MAPK signaling pathway activation in hippocampal neurons of adolescent mice under low temperature conditions (4 °C for 12 h) with western blotting and immunohistochemistry.

or Suppresses NF-κB Signaling Pathway and Protects against AFB₁-Induced Hepatitis: A Novel Potential Preventive Strategy for Aflatoxicosis?

Aflatoxin B₁ (AFB₁), a mycotoxin found in food and feed, is immunotoxic to animals and poses significant threat to the food industry and animal production. The primary target of AFB₁ is the liver. To overcome aflatoxin toxicity, probiotic-mediated detoxification has been proposed.

HMGB1-mediated differential response on hippocampal neurotransmitter disorder and neuroinflammation in adolescent male and female mice following cold exposure.

Stress induces many different sex-specific physiological and psychological responses during adolescence. Although the impact of certain brain stressors has been reported in the literature, the influence of cold stress on the mechanisms underlying hippocampal neurotransmitter disorder and neuroinflammation remain unstudied. Adolescent male and female C57BL/6 mice were exposed to 4 °C temperatures, 3 h per day for 1 week.

Possible mechanisms of prenatal cold stress induced-anxiety-like behavior depression in offspring rats.

Environmental factors and prenatal stress have long-term effects on offspring behavior, physical development, hypothalamic-pituitary-adrenal (HPA) axis regulation, immune activity, and disease susceptibility. To further understand the effects of prenatal cold stress on offspring, we investigated the behavior change; the expression of glucocorticoid receptor (GR), mineralocorticoid receptor (MR), brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 receptor (IGF1R), neuronal nuclei (NEUN), glial fibrillary acidic protein (GFAP), corticotropin-releasing hormone receptor 1 (CRHR1), Gamma-aminobutyric acid B receptor, 2 (GABAB2) proteins in hippocampus; the ratio of CD4/CD8 lymphocyte subsets and the level of norepinephrine (NE), dopamine (DA) in the peripheral blood of weaned offspring rats using behavioral tests and biology analysis methods. The results showed that prenatal cold stress affected offspring HPA axis activity, inhibited the expression of MR, BDNF and IGF1R in the hippocampus of male offspring, and lowered the expression of GR in female offspring.