生理学报最新文献

{"title":"[Effect of GLP-1 on MNCs activity in hypothalamic paraventricular nucleus <i>in vitro</i> in rats].","authors":"Xin Jin, Li Chen, Chun-Ping Chu, Yu-Zi Li, Peng Ren, De-Lai Qiu","doi":"10.13294/j.aps.2026.0042","DOIUrl":"10.13294/j.aps.2026.0042","url":null,"abstract":"<p><p>Glucagon-like peptide-1 (GLP-1) in the brain is synthesized by preproglucagon neurons and released through axonal projections to extensive regions such as the arcuate nucleus, hypothalamic paraventricular nucleus (PVN), rostral ventrolateral medulla, and dorsomedial medulla. It is involved in functional activities including substance metabolism, neuroendocrine regulation, and autonomic nerve control. The GLP-1 receptor (GLP-1R) is highly expressed in the PVN and plays an important role in stress responses and cardiovascular activities. However, the mechanism by which GLP-1 influences the activity of magnocellular neurosecretory cells (MNCs) in the hypothalamic PVN remains unclear. In this study, we used whole-cell patch-clamp recording in acute hypothalamic slices, biotin staining, double immunofluorescence staining, and neuropharmacology methods to investigate the regulatory mechanism of GLP-1 on the activity of the hypothalamic PVN MNCs <i>in vitro</i> in rats. Under current-clamp conditions, perfusion with GLP-1 (100 nmol/L) resulted in a significant decrease in the spontaneous firing frequency of PVN MNCs accompanied with a membrane potential hyperpolarization. Blocking ionotropic glutamate receptors and GABA_A receptors either alone or simultaneously did not affect the inhibitory effect of GLP-1 on the firing frequency of PVN MNCs. GLP-1 had no significant impact on the half-width, rise constant, or decay constant of action potentials, but it significantly increased the after-hyperpolarization (AHP) and inwardly rectifying potassium currents of PVN MNCs. The results of double immunofluorescence showed that GLP-1 significantly reduced the expression of c-fos in arginine vasopressin (AVP)-ergic neurons. These results indicate that GLP-1 activates postsynaptic inwardly rectifying potassium channels, reduces the excitability of PVN MNCs, and decreases their firing frequency and c-fos expression. These findings suggest that GLP-1 reduces the secretion and release of AVP by inhibiting the functional activity of PVN MNCs in rats.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"642-652"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Effects of repeated controlled ovarian stimulation on the expression of aerobic glycolysis-related enzymes at various stages of early embryo development in mice].","authors":"Lu-Lu Shen, Bei-Bei Shi, Wen-Yan Xiong, Rui-Gan Shi, Ya-Jing Song, Hui-Lan DU","doi":"10.13294/j.aps.2026.0026","DOIUrl":"10.13294/j.aps.2026.0026","url":null,"abstract":"<p><p>This study aims to investigate whether the reduction in early embryonic development due to repeated controlled ovarian stimulation (COS) is associated with the expression levels of enzymes related to aerobic glycolysis. A repeated COS mouse model was established by injecting pregnant mare serum gonadotropin (PMSG) followed by human chorionic gonadotrophin (HCG) 48 h later in ICR mice. Repeated COS was performed by repeating this injection protocol. After pregnancy in these mice, 2- to 8-cell embryos and blastocysts were collected. The mRNA and protein expression levels of aerobic glycolysis-related enzymes, including hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA), as well as glucose transporter type 1 (GLUT1) and monocarboxylate transporter 4 (MCT4), were detected at each stage using qRT-PCR and immunofluorescence methods, along with the high-quality embryo rate. The results showed that, compared with the control group, there was no statistically significant difference in the high-quality embryo rate at each stage after a single stimulation (<i>P</i> > 0.05). As the number of stimulation cycles increased, embryo morphology deteriorated, and the high-quality embryo rate decreased. At the 2- to 8-cell stage, compared with the control group, a single stimulation had no significant effect on the mRNA and protein expression levels of HK2, PFK, PKM2, LDHA, GLUT1, and MCT4. However, two stimulations reduced the mRNA expression levels of PFK, PKM2, and GLUT1 at the 2-cell stage, the protein expression level of PFK, and also decreased the mRNA expression levels of LDHA and MCT4 and the protein expression levels of PKM2 and MCT4 at the 4-cell stage, as well as the mRNA and protein expression levels of PFK, LDHA, and MCT4 at the 8-cell stage. Three and four stimulations resulted in decreased mRNA and protein expression levels of HK2, PFK, PKM2, LDHA, GLUT1, and MCT4 at the 2-, 4-, and 8-cell stages (<i>P</i> < 0.05). At the blastocyst stage, a single stimulation had no significant effect on the mRNA and protein expression levels of HK2, PFK, PKM2, LDHA, GLUT1, and MCT4. Two stimulations reduced the protein expression level of LDHA, while three and four stimulations led to decreased mRNA and protein expression levels of HK2, PFK, PKM2, LDHA, GLUT1, and MCT4. These findings indicate that repeated COS reduces the expression levels of aerobic glycolysis-related enzymes at various stages of early embryonic development. Our results suggest that the reduction in early embryonic development due to repeated COS may be associated with the inhibition of aerobic glycolysis.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"592-604"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Gut-brain axis and Parkinson's disease: research progress on the gut-brain interaction].","authors":"Yu-Rui Zhao, Hao-Jun You, Jing Lei","doi":"10.13294/j.aps.2026.0021","DOIUrl":"10.13294/j.aps.2026.0021","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by motor dysfunction. The main pathological manifestations are abnormal accumulation of α-synuclein (α-Syn) in substantia nigra neurons and loss of dopaminergic neurons (DAn). Gastrointestinal (GI) symptom is one of the common non-motor symptoms in PD. It is known that the brain and gut communicate via the parasympathetic nerves and the enteric nervous system (ENS), forming a bidirectional pathway called the gut-brain axis. Dysbiosis of the gut microbiota may be a key driver in the origin and pathological progression of PD, playing an important role in the spread of pathological α-Syn to the central nervous system (CNS) and thereby promoting the progression of PD. This article reviews the mechanism of gut microbiota dysbiosis in the pathogenesis and progression of PD, including its effects on intestinal barrier integrity, neuroinflammation, and pathological α-Syn transmission, and discusses the diagnosis and therapeutic strategies targeting the gut-brain axis, including microbiota transplantation, vagus nerve stimulation, Toll-like receptor 4 (TLR4) antagonists, exercise training, <i>etc</i>., providing new insights for the diagnosis and treatment of PD.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"501-512"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Exploring the regulatory mechanism of <i>Sparassis latifolia</i> polysaccharides on hepatic glucose metabolism disorders in mice based on transcriptomics].","authors":"Er-Chen Yang, Feng-Ying Jia, Li-Min Zhang, Li-Yang Jin, Dao-Qin Ren, Yue Jiang, Shao-Jun Yun, Cui-Ping Feng","doi":"10.13294/j.aps.2026.0058","DOIUrl":"10.13294/j.aps.2026.0058","url":null,"abstract":"<p><p>This study aimed to investigate the effects and mechanism of <i>Sparassis latifolia</i> polysaccharides (SLPs) on hepatic glucose metabolism disorders induced by a high-fat diet combined with streptozotocin (STZ) in mice. A mouse model of hepatic glucose metabolism disorder was established and treated with different doses of SLPs (100, 200, and 400 mg/kg) via gavage for 8 weeks, alongside control, model, and positive control groups (metformin hydrochloride). The effects of SLPs were systematically evaluated through pyruvate tolerance tests (PTT), hepatic glycogen content measurement, liver histomorphological analysis (HE and oil red O staining), transcriptomics, and validation of key signaling pathways using RT-qPCR and Western blot. The results showed that, compared to the model group, medium and high doses of SLPs significantly reduced area under the curve (AUC) of PTT, increased hepatic glycogen content, and ameliorated liver histopathological damage and lipid accumulation in the liver. Transcriptomic analysis revealed that SLPs intervention significantly modulated differentially expressed genes related to glucose and lipid metabolism, which were enriched in signaling pathways such as phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/forkhead box O1 (FOXO1) signaling pathway. Further validation demonstrated that SLPs up-regulated mRNA expression levels of insulin-like growth factor 1 receptor (<i>IGF1R</i>), protein kinase B2 (<i>AKT2</i>), and phosphatidylinositol-3-kinase regulatory subunit 1 (<i>PIK3R1</i>) in the liver of mice with glucose metabolism disorders, and down-regulated the mRNA expression levels of <i>FOXO1</i> and fructose-1,6-bisphosphatase 1 (<i>FBP1</i>). Additionally, SLPs up-regulated p-FOXO1 protein expression level and down-regulated phosphoenolpyruvate carboxykinase (PEPCK) protein expression level. These results suggest that SLPs can effectively improve hepatic glucose metabolism disorders in mice induced by a high-fat diet combined with STZ by activating the PI3K/AKT/FOXO1 signaling pathway, involving the inhibition of key gluconeogenic enzymes and promotion of glucose utilization.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"653-664"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Molecular mechanism of intervertebral disc cell senescence: telomeres, mitochondria, and cellular metabolic reprogramming].","authors":"Wei Deng, Ruo-Chen Zhu, Fan-Guo Kong, Ji-Yao Luan","doi":"10.13294/j.aps.2026.0044","DOIUrl":"10.13294/j.aps.2026.0044","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IVDD), as a common spinal disorder, is closely associated with intervertebral disc cell senescence in its pathogenesis. Cellular senescence leads to alterations in the biomechanical properties of intervertebral discs and causes clinical symptoms including chronic pain and functional impairment. Current research demonstrates that telomere shortening, mitochondrial dysfunction, and cellular metabolic reprogramming constitute the core molecular mechanisms underlying intervertebral disc cell senescence. This review systematically examines the molecular mechanisms of intervertebral disc cell senescence, analyzes the roles of telomere dynamics, mitochondrial homeostasis imbalance, and metabolic reprogramming in this process, and summarizes corresponding potential therapeutic strategies. By elucidating these molecular mechanisms, this work provides a theoretical foundation for developing therapeutic targets to delay IVDD.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"566-578"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The research progress and outlook on the effects of different exercise modalities on working memory function in middle-aged and elderly individuals].","authors":"Yi-Kun Zheng, Zu-Lin Chen, Li-Han Lin, Jie Zheng, Guo-Peng Hu","doi":"10.13294/j.aps.2025.0087","DOIUrl":"10.13294/j.aps.2025.0087","url":null,"abstract":"<p><p>This review provides a comprehensive analysis of the effects of different exercise modalities on working memory function in middle-aged and older adults. It systematically reviews evidence from interventions including aerobic exercise, resistance training, and traditional mind-body exercises, examining their acute effects and long-term mechanisms of action. The findings indicate that aerobic exercise enhances working memory by improving cerebral blood flow, promoting neuroplasticity, and upregulating brain-derived neurotrophic factor (BDNF) levels. Resistance training activates neuroadaptive remodeling mechanisms and optimizes cerebral hemodynamics, thereby strengthening executive control. Traditional mind-body exercises improve the efficiency of cognitive control networks by restructuring functional neural networks and modulating the stress-inflammation axis. Combined exercise regimens, which integrate the synergistic effects of aerobic and resistance training, can further improve working memory performance. Mechanistic studies indicate that exercise interventions optimize neural network function through multiple pathways, including BDNF-mediated synaptic plasticity enhancement, coordinated regulation of the dopaminergic/noradrenergic systems, and improvements in cerebral blood flow and vascular reactivity. A dynamic individualized prescription design based on physiological and cognitive baseline characteristics may maximize cognitive health benefits. Future research should integrate multimodal neuroimaging technologies to clarify the neural mechanisms underlying exercise interventions and develop artificial intelligence-driven personalized prescription systems. At the policy level, integrating sports and medical services and promoting the large-scale application of exercise interventions in populations with multimorbidity are critical to addressing the public health challenges associated with population aging.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"513-535"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress on hepatokines in metabolic dysfunction-associated steatotic liver disease].","authors":"Cheng-Ya Huang, Su-Su DU, Wen Zheng, Xiao-Nan Li","doi":"10.13294/j.aps.2026.0041","DOIUrl":"10.13294/j.aps.2026.0041","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by excessive fat accumulation in the liver resulting from metabolic dysfunction. This condition causes hepatic steatosis and inflammatory injury, representing the most common chronic liver disease globally, while its pathogenesis remains incompletely understood. Recent research has identified a class of cytokines secreted by liver cells, known as hepatokines, which hold dual value as biomarkers and therapeutic targets within the pathophysiological regulatory network of MASLD. This review summarizes the 'multiple-hit' hypothesis regarding the pathogenesis and progression of MASLD. It elaborates on the altered levels and specific molecular mechanisms of hepatokines, such as fetuin-A, selenoprotein P, and fibroblast growth factor 21 (FGF21), in pathological processes including glucolipid metabolic disorders, oxidative stress, and inflammatory responses. Furthermore, it outlines the clinical application prospects of using hepatokines as biomarkers for early-stage MASLD in children. This paper highlights the potential value of hepatokines in MASLD intervention and childhood metabolic abnormalities, proposing them as promising targets for the early diagnosis, intervention, and treatment of MASLD and related metabolic diseases.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"476-486"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The role of β₂-adrenergic receptors in ischemic stroke].","authors":"Shuang Zhang, Ke Wang, Yue Wang, Qian-Qian Liu, Zhi He","doi":"10.13294/j.aps.2025.0110","DOIUrl":"10.13294/j.aps.2025.0110","url":null,"abstract":"<p><p>Ischemic stroke is a common cerebrovascular disease with an increasing incidence year by year, and it remains one of the leading causes of death and disability worldwide. The β₂-adrenergic receptor (β₂-AR), a member of the G protein-coupled receptor (GPCR) family, functions on the cell membrane by binding to specific ligands such as epinephrine (E) and norepinephrine (NE), thereby regulating intracellular signal transduction. Recent studies have revealed that the β₂-AR signaling pathway exerts multifaceted neuroprotective effects on ischemic stroke, including promoting the secretion of neurotrophic factors, mitigating inflammatory responses, inhibiting apoptosis, reducing excitotoxicity, and repairing the blood-brain barrier. Furthermore, research suggests that β₂-AR activation plays a role in post-stroke pneumonia. Additionally, β₂-AR gene polymorphisms have been significantly associated with the risk of ischemic stroke. This article reviews the mechanisms of the β₂-AR signaling pathway in ischemic stroke, aiming to provide a theoretical foundation for the prevention and treatment of this condition.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"270-282"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress of sleep-wake neural circuit mediated by hypothalamus].","authors":"Bin-Hao Long, Ting-Ting Dou, Cui Ma, Yu-Ting Wei, Si-Rui Ma, Xing-Ke Yan","doi":"10.13294/j.aps.2026.0023","DOIUrl":"10.13294/j.aps.2026.0023","url":null,"abstract":"<p><p>The hypothalamus is a critical central hub for regulating sleep-wake patterns in organisms, maintaining the balance between daily activity and rest by modulating sleep-wake-related neural circuits. This article reviews research on hypothalamus-mediated neural circuits involved in sleep-wake regulation. Studies demonstrate that activating specific neuronal subtypes in the lateral hypothalamic area (LHA), paraventricular nucleus of the hypothalamus (PVH), supramammillary nucleus (SuM), preoptic area (POA) and its subregions, and dorsomedial hypothalamic nucleus (DMH) can induce sleep or wakefulness through distinct circuit mechanisms. At the same time, the limitations of the traditional sleep-wake flip-flop model are discussed, along with the supplements and hypotheses. Multiple hypothalamic nuclei form extensive connections with other brain regions, collectively establishing a sophisticated neural architecture that drives wakefulness and stabilizes sleep. This finely tuned regulatory system enables precise control of sleep-wake states, offering foundational insights into the neural mechanisms of sleep-wake transitions and informing potential therapeutic strategies for sleep disorders.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"283-294"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Renal sodium transporters in salt-sensitive hypertension].","authors":"Cheng-Bin Tang, Wen-Hao Chen, Chun-Ling Li, Wei-Dong Wang","doi":"10.13294/j.aps.2026.0035","DOIUrl":"10.13294/j.aps.2026.0035","url":null,"abstract":"<p><p>Hypertension is one of the most important risk factors for cardiovascular, cerebrovascular and renal diseases. The molecular mechanism of hypertension is not fully understood largely due to the complexity of pathogenesis involving many factors. The balance of sodium in body fluids plays a key role in blood pressure regulation. High salt intake is an important environmental factor leading to the development of hypertension. In this setting, the kidney plays a major role in the maintenance of blood pressure. The present review aims to summarize the current overview on the involvement of sodium transporters, sodium exchangers and sodium channels in the modulation of blood pressure, including sodium-hydrogen exchanger isoform 3 (NHE3), Na⁺-K⁺-2Cl^- cotransporter type 2 (NKCC2), sodium-chloride cotransporter (NCC) and epithelial sodium channel (ENaC), which are expressed in different nephron segments and the collecting ducts, respectively. In particular, recent findings on experimental animal models with modified gene of renal ion channels/transporters leading to the identification of several crucial physiological mechanisms involved in hypertension, were also reviewed. These findings could potentially provide novel therapeutic approaches applicable for hypertension.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"253-269"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}