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Abnormal shifts in global climate, leading to extreme weather, significantly threaten the safety of individuals involved in outdoor activities. Hypothermia-induced coma or death frequently occurs in clinical and forensic settings. Despite this, the precise mechanism of central nervous system injury due to hypothermia remains unclear, hindering the development of targeted clinical treatments and specific forensic diagnostic indicators. The GEO database was searched to identify datasets related to hypothermia. Post-bioinformatics analyses, DEGs, and ferroptosis-related DEGs (FerrDEGs) were intersected. GSEA was then conducted to elucidate the functions of the Ferr-related genes. Animal experiments conducted in this study demonstrated that hypothermia, compared to the control treatment, can induce significant alterations in iron death-related genes such as PPARG, SCD, ADIPOQ, SAT1, EGR1, and HMOX1 in cerebral cortex nerve cells. These changes lead to iron ion accumulation, lipid peroxidation, and marked expression of iron death-related proteins. The application of the iron death inhibitor Ferrostatin-1 (Fer-1) effectively modulates the expression of these genes, reduces lipid peroxidation, and improves the expression of iron death-related proteins. Severe hypothermia disrupts the metabolism of cerebral cortex nerve cells, causing significant alterations in ferroptosis-related genes. These genetic changes promote ferroptosis through multiple pathways.

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Apoptosis is a regulated cell death that depends on caspases. It has mainly been studied as a mechanism for the removal of unwanted cells. However, apoptotic cells can induce fate or behavior changes of their neighbors and thereby participate in development. Here, we address the functions of apoptosis during metamorphosis of the cnidarian Hydractinia symbiolongicarpus. We describe the apoptotic profile during metamorphosis of the larva and identify Caspase3/7a, but no other executioner caspases, as essential for apoptosis in this context. Using pharmacological and genetic approaches, we find that apoptosis is required for normal head development. Inhibition of apoptosis resulted in defects in head morphogenesis. Neurogenesis was compromised in the body column of apoptosis-inhibited animals but there was no effect on the survival or proliferation of stem cells, suggesting that apoptosis is required for cellular commitment rather than for the maintenance of their progenitors. Differential transcriptomic analysis identifies TRAF genes as downregulated in apoptosis-inhibited larvae and functional experiments provide evidence that they are essential for head development. Finally, we find no major role for apoptosis in head regeneration in this animal, in contrast to the significance of apoptosis in Hydra head regeneration.

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Numerous studies have demonstrated that neuron-specific enolase (NSE) serves as a distinctive indicator of neuronal injury, with its concentration in blood reflecting the extent and magnitude of nervous system damage, and the expression of serum NSE is correlated with cognitive dysfunction. The assessment of NSE holds significant importance in diagnosing cognitive dysfunction, assessing disease severity, predicting prognosis, and guiding treatment. In this review, the research progress of NSE in cognitive dysfunction was reviewed, and the value of serum NSE level in predicting disease severity and prognosis of patients with cognitive dysfunction was discussed.

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BACKGROUND: Glutamate and glutamine are the most abundant amino acids in the blood and play a crucial role in cell survival in the nervous system. Various transporters found in cell and mitochondrial membranes, such as the solute carriers (SLCs) superfamily, are responsible for maintaining the balance of glutamate and glutamine in the synaptic cleft and within cells. This balance affects the metabolism of glutamate and glutamine as non-essential amino acids. AIMS: This review aims to provide an overview of the transporters and enzymes associated with glutamate and glutamine in neuronal cells. DISCUSSION: We delve into the function of glutamate and glutamine in the nervous system by discussing the transporters involved in the glutamate-glutamine cycle and the key enzymes responsible for their mutual conversion. Additionally, we highlight the role of glutamate and glutamine as carbon and nitrogen donors, as well as their significance as precursors for the synthesis of reduced glutathione (GSH). CONCLUSION: Glutamate and glutamine play a crucial role in the brain due to their special effects. It is essential to focus on understanding glutamate and glutamine metabolism to comprehend the physiological behavior of nerve cells and to treat nervous system disorders and cancer.

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BACKGROUND: Hirschsprung's disease (HSCR) is characterized by a dysfunction of enteric neural crest cells (ENCCs) proliferation, migration and premature apoptosis during embryonic development, resulting in aganglionic colon. Our aim is to explore the role of miR-144 with its target gene Transcription Factor AP 4 (TFAP4) in nerve cells in HSCR. METHODS: The relative expression levels of miR-144 in HSCR colon samples were detected by quantitative real-time PCR (RT-qPCR). Western blot assays were conducted to investigate the TFAP4 protein expressing level. The interaction of miR-144 and TFAP4 was predicted with bioinformatics analysis and examined with luciferase reporter assays. Overexpression or knockdown of miR-144 and TFAP4 in 293T and SH-SY5Y cell lines was applied. Cell proliferation, migration and invasion were detected by CCK-8 assays, Transwell migration and invasion assays. Cell cycle and apoptosis was examined by flow cytometric analysis. RESULTS: Downregulation of miR-144 and upregulation of TFAP4 were shown in HSCR. Luciferase reporter assay indicated that miR-144 reduced luciferase activity in 293T and SH-SY5Y transfected with TFAP4-WT-3UTR luciferase reporter and confirmed TFAP4 was the downstream target gene of miR-144. Data showed that miR-144 promoted the cell proliferation, migration and invasion of 293T and SH-SY5Y, while TFAP4 blocked the cell proliferation, migration and invasion. TFAP4 overexpression reversed the miR-144-mediated cell proliferation, migration and invasion of 293T and SH-SY5Y. CONCLUSIONS: Downregulation of miR-144 blocked the cell proliferation and migration of nerve cells via targeting TFAP4 and contributed to the pathogenesis of HSCR. This provides an innovative and candidate target for treatment of HSCR.

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PURPOSE: Highly active antiretroviral therapy (HAART) is an accepted treatment option for patients with virus infection. Mounting evidence indicated that persistent HAART treatment is implicated with increased morbidity of HIV-associated neurocognitive disorders (HAND) in patients. Tenofovir disoproxil fumarate (TDF), a novel nucleotide reverse transcriptase inhibitor (NRTI), was used in patients with HIV co-infected with HBV. And it is still a vital first-line antiretroviral compounds in HAART. However, whether persistent treatment with TDF is involved in HAND development remains to be further elucidated. In this study, we aimed to discuss the neurotoxicity of TDF. METHODS: We used SH-SY5Y cells and primary neuronal cells to evaluate the neurotoxicity of TDF in vitro. The cytotoxicity of TDF on SH-SY5Y cells and primary neuronal cells was evaluated by the cell viability and LDH levels by MTT assay and LDH kit, respectively. Hoechst 33342 staining, TUNEL assay and flow cytometry were performed to evaluate the cells apoptosis. The intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) production were measured by commercial kits. In addition, the activation level of caspase-3 was evaluated using spectrophotometry and western blotting. RESULTS: Our results showed that TDF treatment significantly induced cell viability and induced apoptosis of SH-SY5Y cells and primary neuronal cells. Furthermore, the ROS levels and MDA productions were significantly up-regulated in nerve cells treated with TDF.  CONCLUSION: Our findings indicated that TDF may induce neuronal cell apoptosis through increasing the intracellular ROS and the expression level of caspase-3, which may be related to the increasing prevalence of HAND.

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Cone photoreceptor cells are wavelength-sensitive neurons in the retinas of vertebrate eyes and are responsible for color vision. The spatial distribution of these nerve cells is commonly referred to as the cone photoreceptor mosaic. By applying the principle of maximum entropy, we demonstrate the universality of retinal cone mosaics in vertebrate eyes by examining various species, namely, rodent, dog, monkey, human, fish, and bird. We introduce a parameter called retinal temperature, which is conserved across the retinas of vertebrates. The virial equation of state for two-dimensional cellular networks, known as Lemaître's law, is also obtained as a special case of our formalism. We investigate the behavior of several artificially generated networks and the natural one of the retina concerning this universal, topological law.

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Brain-derived nerve factor (BDNF), through TrkB receptor activation, is an important modulator for many different physiological and pathological functions in the nervous system. Among them, BDNF plays a crucial role in the development and correct maintenance of brain circuits and synaptic plasticity as well as in neurodegenerative diseases. The proper functioning of the central nervous system depends on the available BDNF concentrations, which are tightly regulated at transcriptional and translational levels but also by its regulated secretion. In this review we summarize the new advances regarding the molecular players involved in BDNF release. In addition, we will address how changes of their levels or function in these proteins have a great impact in those functions modulated by BDNF under physiological and pathological conditions.

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Currently, more and more patients suffer from peripheral nerve injury due to trauma, tumor and other causes worldwide. Biomaterial-based nerve conduits are increasingly recognized as a potential alternative to nerve autografts for the treatment of peripheral nerve injury. However, an ideal nerve conduit must offer topological guidance and biochemical and electrical signal transduction mechanisms. In this work, aligned conductive nanofibrous scaffolds comprising polylactic-co-glycolic acid and multiwalled carbon nanotubes (MWCNTs) were fabricated via coaxial electrospinning, and nerve growth factor (NGF) and Lycium barbarum polysaccharides (LBP) purified from the wolfberry were loaded on the core and shell layers of the nanofibers, respectively. LBP were confirmed to accelerate long-distance axon regeneration after severe peripheral nerve injury. In addition, the synergistic promotion of LBP and NGF on nerve cell proliferation and neurite outgrowth was demonstrated. MWCNTs were introduced into the aligned fibers to further increase the electrical conductivity, which promoted the directional growth and neurite extension of neurons in vitro. Further, the combination of conductive fibrous scaffolds with electrical stimulation that mimics endogenous electric fields significantly promoted the differentiation of PC12 cells and the axon outgrowth of neurons. Based on robust cell-induced behaviors, conductive composite fibers with optimized fiber alignment may be used for the promotion of nerve recovery.

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Ischemic stroke is the second leading cause of human death and the third reason of disability. Meanwhile, the incidence is rising year after year worldwide. Ischemic stroke could cause ischemia-reperfusion injury after blood recanalization treat-ment, but the mechanism of ischemia-reperfusion injury is still not very clear, so it is necessary to build a preclinical model with specific characteristics. Up to now, animal experiments have been still complicated, and the culture of brain slices has some limitations. The cell model in vitro has become a simplified and valuable tool widely used by researchers. The paper systematically summarizes the common type of nerve cells, and further analyzes establishment methods and principle, relevant research progress on the in vitro model of ischemia-reperfusion, in order to provide reference for rationally selecting hypoxia and reoxygenation model for basic research on cerebral ischemia and reperfusion and drug screening.

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Lamotrigine (LTG) is a widely used drug for the treatment of epilepsy. Emerging clinical evidence suggests that LTG may improve cognitive function in patients with Alzheimer's disease. However, the underlying molecular mechanisms remain unclear. In this study, amyloid precursor protein/presenilin 1 (APP/PS1) double transgenic mice were used as a model of Alzheimer's disease. Five-month-old APP/PS1 mice were intragastrically administered 30 mg/kg LTG or vehicle once per day for 3 successive months. The cognitive functions of animals were assessed using Morris water maze. Hyperphosphorylated tau and markers of synapse and glial cells were detected by western blot assay. The cell damage in the brain was investigated using hematoxylin and eosin staining. The levels of amyloid-ß and the concentrations of interleukin-1ß, interleukin-6 and tumor necrosis factor-α in the brain were measured using enzyme-linked immunosorbent assay. Differentially expressed genes in the brain after LTG treatment were analyzed by high-throughput RNA sequencing and real-time polymerase chain reaction. We found that LTG substantially improved spatial cognitive deficits of APP/PS1 mice; alleviated damage to synapses and nerve cells in the brain; and reduced amyloid-ß levels, tau protein hyperphosphorylation, and inflammatory responses. High-throughput RNA sequencing revealed that the beneficial effects of LTG on Alzheimer's disease-related neuropathologies may have been mediated by the regulation of Ptgds, Cd74, Map3k1, Fosb, and Spp1 expression in the brain. These findings revealed potential molecular mechanisms by which LTG treatment improved Alzheimer's disease. Furthermore, these data indicate that LTG may be a promising therapeutic drug for Alzheimer's disease.

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Objective:To investigate the effect of long non-coding RNA (lncRNA) human histocompatibility leukocyte antigen complex P5 (HCP5) on the neuronal injury induced by oxygen glucose deprivation/reoxygenation (OGD/R), and to analyze its potential mechanism.Methods:SH-SY5Y cells were divided into control group (CON group, normal medium culture), model group (Model group, OGD/R), interference control group (si-NC group, OGD/R after HCP5 small interfering RNA negative control (si-NC)), HCP5 interference group (si-HCP5 group, OGD/R after HCP5 small interfering RNA (si-HCP5)), HCP5 interference+ inhibitor control group (si-HCP5+ anti-NC group, OGD/R after transfection of si-HCP5, miR-525-5p inhibitor negative control (anti-NC)), HCP5 interference+ miR-525-5p inhibitor group (si-HCP5+ anti-miR-525-5p group, OGD/R after transfection of si-HCP5, miR-525-5p inhibitor). qRT-PCR was used to detect the expression of lncRNA HCP5 and miR-525-5p in cells.The activity of SH-SY5Y cells was detected by MTT.The level of reactive oxygen species (ROS) in the cells was detected by fluorescent probe of dichlorofluorescein diacetate (DCFH-DA). The apoptosis of SH-SY5Y cells was detected by flow cytometry.Western blot was used to detect the expression of BTG2, Bcl-2 related X protein (Bax), B lymphocyte tumor 2 (Bcl-2) and cleaved caspase-3 protein.SPSS 25.0 software was used to analyze the data, and one-way ANOVA was used for comparison between multiple groups, and SNK- q test was used for further comparison between two groups. Results:There were statistically significant differences in lncRNA HCP5, miR-525-5p RNA levels and BTG2 protein expression levels among the 6 groups ( F=28.853, 59.241, 13.731, all P<0.001). Compared with the CON group, the Model group had higher level of lncRNA HCP5, lower level of miR-525-5p, and higher level of BTG2 protein (all P<0.05). Compared with the Model group, the si-HCP5 group had lower level of lncRNA HCP5, higher level of miR-525-5p, and lower level of BTG2 protein (all P<0.05). Compared with the si-HCP5+ anti-NC group, the si-HCP5+ anti-miR-525-5p group had higher level of lncRNA HCP5, lower level of miR-525-5p, and higher level of BTG2 protein (all P<0.05). There were statistically significant differences in cell activity and ROS levels among the six groups of cells ( F=16.180, 59.950, both P<0.001). The cell activity of the Model group was lower than that of the CON group (0.33±0.12, 0.63±0.11) ( P<0.05), and the ROS level was higher than that of the CON group (224.62±23.27, 100.00±0.00) ( P<0.05). The cell activity of the si-HCP5+ anti-miR-525-5p group was lower than that of the si-HCP5+ anti-NC group (0.38±0.08, 0.58±0.08) ( P<0.05), and the ROS level was higher than that of the si-HCP5+ anti-NC group (207.83±19.39, 135.27±14.36) ( P<0.05). There were statistically significant differences in the apoptosis rate and expression levels of apoptotic proteins Bcl-2, Bax, and cleared Caspase-3 among the six groups of cells ( F=27.994, 29.660, 45.000, 52.983, all P<0.001). There were no statistically significant difference in Bax, Bcl-2, cleared Caspase-3 protein levels, and apoptosis rate in SH-SY5Y cells between the Model group and the si-NC group, as well as between the si-HCP5 group and the si-HCP5+ anti-NC group (all P>0.05). Compared with the CON group, the apoptosis rate, levels of Bax and cleared Casase-3 protein in the Model group were significantly upregulated (all P<0.05), while the Bcl-2 protein level was significantly downregulated ( P<0.05). Compared with the Model group and si-NC group, the si-HCP5 group showed significant downregulation of cell apoptosis rate and levels of Bax and cleared Caspase-3 protein (all P<0.05), while the Bcl-2 protein level was upregulated ( P<0.05). Compared with the si-HCP5 group and si-HCP5+ anti-NC group, the si-HCP5+ anti-miR-525-5p group showed significant upregulation of cell apoptosis rate and levels of Bax and cleared Caspase-3 protein levels (all P<0.05), and significant downregulation of Bcl-2 protein levels ( P<0.05). Conclusion:lncRNA HCP5 may inhibit the expression of BTG2 by targeting up-regulation of miR-525-5p, thus leading to apoptosis of nerve cells in OGD/R models.

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Arm illaria mellea has been known and used in traditional medicine in East Asia for hundreds of years. It has already been reported that A. mellea extracts have various pharmacological effects, and the polysaccharides of A. mellea exhibit antioxidant and anti-apoptotic activities. In this study, a water-soluble polysaccharide (AMP-N-a-1), with an average molecular weight of 17 kD, was isolated and purified from the water extract of A. mellea using DEAE-52, Sepharose CL-4B, and Sephadex G-100 column chromatography. AMP-N-a-1 was mainly composed of Man (1.65%), Glca (1.64%), Rha (1.82%), Gala (2.49%), Glc (90.48%), Gal (0.89%), Xyl (0.42%), and Ara (0.61%). AMP-N-a-1 was used to study the effect on the learning and memory of mice and its underlying mechanisms. The results showed that AMP-N-a-1 could significantly increase the activities of catalase (CAT) and superoxide dismutase (SOD) and reduce the content of nitric oxide (NO) in mouse brain tissue. Meanwhile, AMP-N-a-1 could reduce the contents of norepinephrine (NE) and dopamine (DA) but could increase the content of 5-hydroxytryptamine (5-HT) in mouse brain tissue. In addition, the immunofluorescence experiment showed that AMP-N-a-1 could promote the proliferation of hippocampal dentate gyrus neurons. The above results indicate that AMP-N-a-1 can significantly improve the learning and memory of mice, and the mechanism may be that AMP-N-a-1 can participate in the regulation of learning and memory through a variety of ways.

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Previous studies have confirmed that both recombinant human erythropoietin (rhEPO) and peroxisome proliferator-activated receptors γ (PPARγ) activator pioglitazone can protect senescent nerve cells, and their mechanisms involve enhancing cell antioxidant capacity and reducing cell apoptosis. However, whether the PPARγ pathway is involved in the rhEPO anti-aging process in neuronal cells is still unclear. In this study, to explore the relationship between rhEPO and the PPARγ pathway at the cellular level, primary nerve cells cultured for 22 days were used to simulate the natural aging process of nerve cells. Starting on the 11th day of culture, rhEPO, LY294002, and GW9662 were added for treatment. Immunochemical methods and SA-ß-gal staining were used to observe the changes in cellular antioxidant capacity and the fraction of senescent cells. The results showed that PPARγ blockade retarded the effect of rhEPO on the cellular antioxidant capacity and altered the fraction of senescent cells. It was confirmed that PPARγ was involved in rhEPO's anti-aging process in neuronal cells. Real-time fluorescent quantitative RT-PCR, Western blotting, and immunofluorescence staining were used to observe the changes in PPARγ pathway-related factors in nerve cells after rhEPO treatment. The results showed that rhEPO significantly upregulated the expression of PPARγ coactivator-1α (PGC-1α), PPARγ, and nuclear PPARγ in cells but did not affect the level of phosphorylated PPARγ protein, confirming that rhEPO has the ability to upregulate the PPARγ pathway. PI3K/Akt and PPARγ pathway blockade experiments were used to explore the relationships among rhEPO, PI3K/Akt, and PPARγ. The results showed that after PPARγ blockade, rhEPO had no significant effect on the PI3K/Akt pathway-related factor p-Akt, while after PI3K/Akt blockade, rhEPO's effects on PPARγ-related factors (PGC-1α, PPARγ, and nuclear PPARγ) were significantly decreased. It is suggested that rhEPO delays the PI3K/Akt pathway in the process of neuronal senescence, which is located upstream of PPARγ regulation. In conclusion, this study confirmed that rhEPO can upregulate the expression of PGC-1α and PPARγ in cells and the level of PPARγ protein in the nucleus to enhance the antioxidant capacity of cells and delay the senescence of nerve cells through the PI3K/Akt pathway. These findings will provide ideas for finding new targets for neuroprotection research and will also provide a theoretical basis and experimental evidence for rhEPO anti-aging research in neural cells.

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BACKGROUND: To study the protective effect of tauroursodeoxycholic acid (TUDCA) on the spinal cord nerve cells (SCN) of SD rats and to explore the protective mechanism of TUDCA against mechanical injury of the SCN. MATERIAL AND METHODS: The SCN of SD rats were cultured in vitro, and a mechanical injury models of 1 mm, 3 mm, and 5 mm SCN were established. The cell survival rate was determined using the MTT assay to determine the optimal degree and time of injury. Different concentrations (0.5, to 20 mmol/L) of TUDCA were used to detect SCN cell survival rate after mechanical injury. MTT assay was used to determine the optimal TUDCA intervention dose. SCN autophagy in different experimental groups were observed by electron microscopy after the best degree of mechanical injury, time of injury, and TUDCA concentration. Beclin-1 and LC3 II/I expressions were detected by western blotting and immunohistochemistry. RESULTS: Survival rate of SCN was close to 50% when the injury interval was 3 mm and the injury time was 24 h, significantly different from those of each group (P < 0.05). At 3 mm injury interval and 24 h injury time, SCN survival rate was approximately 80% when TUDCA concentration was 4 mmol/L, which was significantly different from those of each group (P < 0.05). Cell morphology of the normal control group was complete, with few autophagy lysosomes. Compared with the normal control group, the number of autophagic lysosomes in the mechanical injury group increased, and cell damage was more severe. Compared with the mechanical injury group, the number of autophagy lysosomes in the mechanical injury + TUDCA intervention group increased significantly, and cell damage was less severe. Further, compared with the normal control group, beclin-1 and lc3ii / I expressions in the mechanical injury group were significantly higher (P < 0.05); compared with the mechanical injury group, beclin-1 and lc3ii / I expressions in the mechanical injury + TUDCA intervention group were significantly higher (P < 0.05). CONCLUSION: TUDCA can protect SCN from mechanical injury in vitro, which may be related to the enhancement of the expression of autophagy-related protein beclin-1 and LC3 II/I.

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miR-101a-3p is expressed in a variety of organs and tissues and plays a regulatory role in many diseases, but its role in spinal cord ischemia/reperfusion injury remains unclear. In this study, we established a rat model of spinal cord ischemia/reperfusion injury by clamping the aortic arch for 14 minutes followed by reperfusion for 24 hours. Results showed that miR-101a-3p expression in L4-L6 spinal cord was greatly decreased, whereas MYCN expression was greatly increased. Dual-luciferase reporter assay results showed that miR-101a-3p targeted MYCN. MYCN immunoreactivity, which was primarily colocalized with neurons in L4-L6 spinal tissue, greatly increased after spinal cord ischemia/reperfusion injury. However, intrathecal injection of an miR-101a-3p mimic within 24 hours before injury decreased MYCN, p53, caspase-9 and interleukin-1ß expression, reduced p53 immunoreactivity, reduced the number of MYCN/NeuN-positive cells and the number of necrotic cells in L4-L6 spinal tissue, and increased Tarlov scores. These findings suggest that the miR-101a-3p mimic improved spinal ischemia/reperfusion injury-induced nerve cell apoptosis and inflammation by inhibiting MYCN and the p53 signaling pathway. Therefore, miR-101a-3p mimic therapy may be a potential treatment option for spinal ischemia/reperfusion injury.

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Kazakh sheep are typical seasonal estrus animals. Their reproductive system regulation mainly involves the complex regulation of the hypothalamic-pituitary-gonadal axis (HPGA), which is also closely related to reproductive hormone secretion. Gonadotropin-releasing hormone (GnRH), synthesized and secreted by the hypothalamus, is the key to controlling sheep reproductive activity. We studied how GNAQ (G protein subunit alpha q) regulates estrus in sheep by controlling GnRH expression and secretion. We used hypothalamic nerve cells as the research model. GNAQ overexpression and RNA interference vectors were constructed and transfected into the hypothalamic nerve cells of fetal Kazakh sheep. qPCR, western blotting, and enzyme-linked immunosorbent assay were used to detect GNAQ gene expression in Kazakh ewe tissues and analyze its regulatory effect on GnRH expression in the hypothalamic nerve cells. The fetal sheep hypothalamic nerve cells were successfully isolated and cultured. qPCR and cell immunofluorescence showed that the purity of positive cells was >95%. The tissue expression profile showed that there were different degrees of GNAQ gene expression in the Kazakh ewe tissue. Expression levels were relatively higher in the hypothalamus, pituitary, brain, and uterine tissues. When GNAQ expression was downregulated in the hypothalamic nerve cells, the upstream genes KISS1 (kisspeptin), GPR54 (KISS1 receptor), and ER (estrogen receptor) were all upregulated, as were the downstream genes PLCB1 (phospholipase C beta 1), PRKCB (protein kinase C beta), and GNRH. At the same time, GnRH secretion levels were also upregulated. GNAQ regulated its downstream gene PLCB1 in the hypothalamic nerve cells, and directly regulated GnRH expression and secretion through the calcium and PRKC signaling pathways. GNAQ also regulated kisspeptin expression, subsequently regulating GnRH expression and secretion indirectly through the kisspeptin-GPR54 signaling pathway. Our results are of great importance for improving the reproductive performance of seasonal-estrus sheep.

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Experts have proven that photobiological regulation therapy for spinal cord injury promotes the spinal repair following injury. The traditional irradiation therapy mode is indirect (percutaneous irradiation), which could significantly lower the effective use of light energy. In earlier studies, we developed an implantable optical fiber that one can embed above the spinal cord lamina, and the light directly is cast onto the surface of the spinal cord in a way that can dramatically improve energy use. Nonetheless, it remains to be seen whether near-infrared light diffused by embedded optical fiber can have side effects on the surrounding nerve cells. Given this, we implanted optical fiber on the lamina of a normal spinal cord to observe the structural integrity of the tissue using morphological staining; we also used immunohistochemistry to detect inflammatory factors. Considering the existing studies, we meant to determine that the light energy diffused by embedded optical fiber has no side effect on the normal tissue. The results of this study will lay a foundation for the clinical application of the treatment of spinal cord injury by near-infrared light irradiation.

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To maintain energy supply to the brain, a direct energy source called adenosine triphosphate (ATP) is produced by oxidative phosphorylation and aerobic glycolysis of glucose in the mitochondria and cytoplasm. Brain glucose metabolism is reduced in many neurodegenerative diseases, including Alzheimer's disease (AD), where it appears presymptomatically in a progressive and region-specific manner. Following dysregulation of energy metabolism in AD, many cellular repair/regenerative processes are activated to conserve the energy required for cell viability. Glucose metabolism plays an important role in the pathology of AD and is closely associated with the tricarboxylic acid cycle, type 2 diabetes mellitus, and insulin resistance. The glucose intake in neurons is from endothelial cells, astrocytes, and microglia. Damage to neurocentric glucose also damages the energy transport systems in AD. Gut microbiota is necessary to modulate bidirectional communication between the gastrointestinal tract and brain. Gut microbiota may influence the process of AD by regulating the immune system and maintaining the integrity of the intestinal barrier. Furthermore, some therapeutic strategies have shown promising therapeutic effects in the treatment of AD at different stages, including the use of antidiabetic drugs, rescuing mitochondrial dysfunction, and epigenetic and dietary intervention. This review discusses the underlying mechanisms of alterations in energy metabolism in AD and provides potential therapeutic strategies in the treatment of AD.

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AIM: To investigate the effect and molecular mechanism of Phellodendron amurense egtract on hippocampal nerve cells induced be Aβ