Objective To compare the differences in c-Fos protein expression in various brain nuclei of acute itch model mice induced by histamine(His) and chloroquine(CQ), the chronic itch model induced by 1-fluoro-2,4-dinitrofluorobenzene (DNFB), and the chronic kidney disease-associated pruritus (CKD-aP) model, and to explore the common central nervous system nuclei mediating different types of itch stimuli. Methods Mice were divided into His, CQ, DNFB, CKD-aP groups, and respective control groups, with six mice in each group. Immunohistochemical staining was used to label c-FOS protein throughout the brain, followed by quantitative analyses. Results Compared with the control group, c-FOS expression increased in the left/right ventrolateral/medial olivary nucleus (LVPO/MVPO), thalamic reticular nucleus (Re), paraventricular thalamic nucleus (PVT), lateral pallidum (LPB), inferior colliculus (IC), pontine nucleus (Pn), and superior colliculus (SC) showed increased c-FOS expression (P<0.05) compared to the control group, with a higher proportion of c-FOS/ neuronal nuclei（NeuN）double-labeled neurons among NeuN-positive neurons (P<0.05); In the DNFB group, c-FOS expression increased in Pn and SC compared to the control group (P<0.0001), and the proportion of c-FOS/NeuN double-labeled neurons among NeuN-positive neurons was elevated (P<0.001). However, no significant increase in c-FOS protein was observed in LVPO/MVPO, Re, PVT, LPB, or IC; In the CKD-aP group, c-FOS expression increased in the SC compared to the control group (P<0.001), and the proportion of c-FOS/NeuN double-labeled neurons among NeuN-positive neurons was elevated (P<0.0001). However, no significant increase in c-FOS protein was observed in the LVPO/MVPO, Re, PVT, LPB, IC, or Pn. Conclusion Acute itch activates the LVPO/MVPO, PVT, Re, IC, LPB, Pn, and SC; DNFB-induced chronic itch activates the Pn and SC; CKD-aP activates the SC. The SC can be activated by acute itch, chronic itch, and systemic disease-related itch, suggesting that the SC may serve as a common downstream center mediating multiple types of itch.

Objective To explore possible healing advantages of probiotics in controlling Alzheimer’s diseese(AD). Methods Conducting an extensive evaluation of probiotics’ healing effects, encompassing various facets and perspectives. We conducted an extensive search across 9 databases with no language restrictions, spanning from the inception of research to March 7, 2025, to identify randomized controlled studies examining the impact of probiotic therapy on. A meta-analysis was then performed using random-effects models to determine the standardized mean difference (SMD), I2 statistic, and 95% confidence interval (CI). Results The study eventually incorporated eight randomized controlled trials (RCT), with 261 individuals in probiotic cohort and 256 in the placebo group. Probiotics significantly improved cognitive function, promoted total anti-oxidant capacity and mitigated the pro-oxidant process and inflammation. Conclusion The significance of probiotic supplements lies in their ability to enhance cognitive abilities in individuals with cognitive deficits, offering both theoretical underpinnings and actionable advice for using probiotics clinically in AD treatment.

Objective To investigate the expression and localization of receptor expression-enhancing protein 2(REEP2) protein throughout the adult mouse brain, providing essential anatomical insights into its physiological functions and mechanistic involvement in hereditary spastic paraplegias (HSP). Methods An integrated approach combining Human Protein Atlas (HPA) database analysis and immunohistochemical techniques were employed. Brain sections from 6 adult mice were used for REEP2 immunohistochemical staining. Whole-brain section imaging was acquired using a digital scanning microscopic imaging system, with precise anatomical identification and localization of positively expressed regions based on the standard mouse brain atlas. Results REEP2 protein was widely expressed in the brains of adult mice, including the cerebral cortex, thalamus, cerebellum, and hippocampus. Localization and analysis of REEP2-positive regions and cells revealed its predominant expression in neuronal cell bodies and dendrites, with all REEP2-positive structures appearing as brownish-yellow granules. Notably, high expression was observed in pyramidal neurons of the cerebral cortex, caudate and putamen neurons of the basal ganglia, the ventral posterior medial and lateral nuclei of the thalamus, and the lateral nucleus group of the thalamus (e.g., the lateral posterior nucleus neurons) as well as cerebellar Purkinje cells. In hippocampal neurons, it showed moderate expression. Conclusion REEP2 protein is enriched in several brain regions, e.g. cortex, cerebellum, striatum, thalamus, hippocampus, etc. This study elucidates the spatial expression profile of REEP2 protein in the adult mouse brain. The findings provide crucial morphological evidence for subsequent development of conditional knockout animal models and further investigation into the role of REEP2 dysfunction in HSP pathogenesis, as well as its broader neural functions.

Objective To investigate the effects of microRNA(miR)-27a on hypoxia-inducible factor 1α (HIF-1α) and the biological activity of human dental pulp stem cells (hDPCs), and to preliminarily explore its potential mechanism based on the PI3K/Akt signaling pathway. Methods Animal experiments: Thirty SPF-grade male SD rats (6-9 months old, weighing 275-310 g) were randomly divided into five groups (n=6 per group): Normal group (Nor),pulpitis group (Pul), no-load group (NL), inhibitor group (Inh), Inh+740Y-P group. The expression level of miR-27a was detected by Real-time PCR. Pathological changes in pulp tissue were observed by HE staining. The levels of related inflammatory factors were detected by ELISA. The expression levels of HIF-1α and PI3K/Akt signaling pathway-related proteins were detected by Western blotting. Cell experiments: hDPCs were randomly divided into five groups, control group (Ctrl), lipopolysaccharidegroup (LPS), negative control inhibitor group（NC inh）, miR-27a inhibitor group (miR-27a inh), miR-27a inhibitor+740Y-P group (miR-27a inh+740Y-P). Cell proliferation and apoptosis rates were detected by CCK-8 assay and flow cytometry, respectively. Results Animal experiment: Compared with the Nor group, the levels of miR-27a, inflammatory cytokines interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, HIF-1α, and proteins related to the PI3K/Akt signaling pathway in the Pul and NL groups increased significantly (P<0.05). The above-mentioned indicators in the Inh group were significantly lower than those in the Pul and NL groups (P< 0.05). Compared with the Inh group, the levels of inflammatory cytokines, HIF-1α, and proteins related to the PI3K/Akt signaling pathway in the Inh+740Y-P group increased significantly (P<0.05). Cell experiments: With the prolongation of LPS treatment time, the expression level of miR-27a in hDPCs gradually increased (P<0.05). Compared with the Ctrl group, the levels of miR-27a, cell apoptosis rate, inflammatory cytokines, HIF-1α protein, and proteins related to the PI3K/Akt signaling pathway in the LPS group and NC inh group increased significantly (P<0.05), while the cell proliferation rate decreased significantly (P<0.05). Compared with the LPS group and NC inh group, the above-mentioned indicators in the miR-27a inh group decreased significantly (P<0.05), and the cell proliferation rate increased significantly (P<0.05). Compared with the miR-27a inh group, the cell apoptosis rate, inflammatory cytokines, HIF-1α protein, and proteins related to the PI3K/Akt signaling pathway in the miR-27a inh + 740Y-P group increased significantly (P<0.05), while the cell proliferation rate decreased significantly (P<0.05). Conclusion MiR-27a can exacerbate the inflammatory response by activating the PI3K/Akt/HIF-1α signaling pathway, thereby affecting the biological activities such as proliferation and apoptosis of dental pulp stem cells and promoting the progression of pulpitis in rats.

Objective To investigate effect of long non-coding RNA small nucleolar RNA host gene 14 (LncRNA SNHG14) on malignant biological behaviors of lung cancer cells by regulating the microRNA-1276 (miR-1276)/methionine adenosyltransferase 2A (MAT2A) axis. Methods Real-time PCR was used to measure SNHG14, miR-1276, and MAT2A mRNA levels in lung cancer tissue, adjacent non-tumor tissues, and in human lung cancer cell lines A549 and NCI-H1299, as well as normal alveolar epithelial cell line BEAS-2B. A549 and NCI-H1299 cells were allocated into the following groups, control(Ctrl), small interfering negative Control (si-NC), si-SNHG14, si-SNHG14 + anti-microRNA negative control (anti-miR-NC), and si-SNHG14 + anti-miR-1276. Colony formation assay and 5-ethynyl-2’-deoxyuridine(EdU)assay were used to assess cell proliferation; Flow cytometry was used to detect apoptosis; Transwell assay was used to assess migration and invasion. Western blotting was used to determine protein expression of Cyclin D1, marker of proliferation Ki-67 (Ki-67), Caspase-3, Bax, and MAT2A. Dual-luciferase reporter assay and RNA pull-down assay were employed to confirm the targeting relationships between SNHG14 and miR-1276, and between miR-1276 and MAT2A. Results Compared with adjacent non-tumor tissue, lung cancer tissue had higher expression of SNHG14 and MAT2A mRNA, and lower expression of miR-1276 (P<0.05). Compared with BEAS-2B cells, A549 and NCI-H1299 cells exhibited higher SNHG14 and MAT2A mRNA levels and lower miR-1276 levels (P<0.05). In si-SNHG14-treated cells, SNHG14 and MAT2A mRNA and protein levels were reduced relative to the si-NC group, along with decreased colony formation rate, EdU positivity, migration and invasion, and lower expression of Cyclin D1 and Ki-67; miR-1276 expression and apoptosis rate, as well as Caspase-3 and Bax protein levels increased (P<0.05). Compared with si-SNHG14 + anti-miR-NC, the si-SNHG14 + anti-miR-1276 group showed increased colony formation, EdU positivity, and numbers of migrating and invading cells, higher MAT2A mRNA expression, and elevated MAT2A, Cyclin D1, and Ki-67 protein levels, while miR-1276 expression, apoptosis rate, and Caspase-3 and Bax protein levels decreased (P<0.05). SNHG14 acted as a molecular sponge to sequester miR-1276, while miR-1276 directly targets and inhibits MAT2A expression. Conclusion Downregulation of LncRNA SNHG14 suppresses malignant biological behaviors of lung cancer cells by modulating the miR-1276/MAT2A axis.

Objective To investigate the effect and mechanism of circular RNA 3-hydroxy-3-methylglutaryl-CoA synthase 1 (circHMGCS1) regulating pancreatic cancer cell proliferation and glycolysis via the microRNA-335-5p（miR-335-5p）/myosin heavy chain 9 (MYH9) pathway. Methods HE staining detected pancreatic cancer tissue morphology; Real-time PCR was used to measure the expression of circHMGCS1, miR-335-5p, and MYH9 mRNA in 17 cases of pancreatic cancer tissue and pancreatic cancer cell lines (PANC-1, Pan02, BXPC-3). PANC-1 cells were divided into: pancreatic cancer group, knockdown control group, circHMGCS1 knockdown group, upregulation control group, miR-335-5p-upregulated group, circHMGCS1-silenced + anti-miR-negative control (NC) group, and circHMGCS1-silenced + anti-miR-335-5p group. Cell proliferation was assessed using colony formation and CCK-8 assays. Glucose uptake and lactate production in the cell supernatant were measured using related kits. Western blotting was performed to detect MYH9, proliferating cell nuclear antigen (PCNA), hexokinase 2 (HK2), and pyruvate kinase M2 (PKM2) protein levels. The regulatory relationship between circHMGCS1 and miR-335-5p/MYH9 was validated. Results Paracancerous tissue showed normal structure, while pancreatic cancer tissue exhibited malignant features such as loss of normal acinar structure, hyperchromatic nuclei, and nuclear pleomorphism. CircHMGCS1 and MYH9 mRNA expression were significantly higher in pancreatic cancer tissues than in adjacent normal tissues, while miR-335-5p expression was significantly lower (P<0.05). In PANC-1, Pan02, and BXPC-3 cells, circHMGCS1 and MYH9 mRNA expression were significantly higher than in H6C7 cells, whereas miR-335-5p expression was significantly lower, with the most pronounced changes observed in PANC-1 cells (P<0.05). After knockdown circHMGCS1 or upregulating miR-335-5p, the expression of MYH9 mRNA, clone formation rate, 450 nm absorbance（A450）value, glucose uptake, lactate production, as well as the protein levels of MYH9, PCNA, HK2, and PKM2 decreased, while the expression of miR-335-5p increased (P<0.05); Anti-miR-335-5p reversed the inhibitory effect of circHMGCS1 knockdown on glycolysis and proliferation of PANC-1 cells. circHMGCS1 targets and regulates miR-335-5p/MYH9. Conclusion CircHMGCS1 may inhibit glycolysis in PANC-1 cells by regulating the miR-335-5p/MYH9 axis, thereby suppressing cell proliferation.

Objective To investigate the mechanism by which leonurus(Leo) improves pulmonary fibrosis in rats with acute respiratory distress syndrome (ARDS) through the AMP-activated protein kinase (AMPK)/ sirtuin 1(SIRT1)/ nuclear factor-κB (NF-κB) pathway. Methods The ARDS model was established by intratracheal instillation of lipopolysaccharide. Forty-eight rats with successful model establishment were randomly divided into four groups, including the ARDS group, the Leo group, the AMPK activator (AICAR) group, and the Leo + AMPK inhibitor compound C (Comp C) group, with 12 rats in each group. Additionally, 12 normal rats were selected as the control(Ctrl) group. Oxygenation index, arterial partial oxygen pressure and lung wet-dry weight ratio were measured. HE and Masson staining were used to detect pulmonary tissue pathology and pulmonary fibrosis. Real-time PCR was used to detect the mRNA expression of pulmonary fibrosis-related genes. ELISA was employed to measure the levels of inflammatory factors, and Western blotting was applied to detect pulmonary fibrosis-related proteins and proteins in the AMPK/SIRT1/NF-κB pathway. Results Compared with the ARDS group, the Leo and the AICAR group exhibited thickened alveolar septa, reduced inflammatory cell infiltration, and decreased deposition of blue-stained collagen fibers. Oxygenation index, arterial partial pressure of oxygen, interleukin (IL)-10 levels, and claudin-5, p-AMPK, AMPK, and SIRT1 protein expression increased significantly. In contrast, lung wet/dry weight ratio, pulmonary mRNA and protein expressions of collagen type Ⅰ (ColⅠ), fibronectin (FN), and α-smooth muscle actin (α-SMA), levels of IL-6 and tumor necrosis factor α(TNF-α), and p-NF-κB p65/NF-κB p65 decreased markedly(P<0.05). Comp C attenuated the ameliorative effect of leonurus on pulmonary fibrosis in ARDS rats. Conclusion Leonurus may improve pulmonary fibrosis in ARDS rats by activating AMPK/SIRT1 to inhibit NF-κB pathway.

Objective To investigate the effect of curcumin (Cur) on myocardial infarction (MI) treated with by bone marrow mesenchymal stem cells (BMSCs) transplantation and to study whether it exerts its effects through endoplasmic reticulum stress (ERS)-related pathways. Methods Forty SD rats were randomly divided into sham-operated group (sham), MI model group (MI), BMSCs transplantation group (BMSCs), and curcumin-pretreated BMSCs transplantation group (Cur). An MI model was established by ligation of the left anterior descending coronary artery. In the sham group, only sutures were threaded without ligation. After modeling, untreated BMSCs or Cur-pretreated BMSCs were injected into the infarct area of the BMSCs group and the Cur group, respectively. Four weeks after transplantation, cardiac function indicators including left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-diastolic volume (LVEDV), and left ventricular end-systolic volume (LVESV) were assessed by echocardiography. Myocardial histopathological changes and fibrosis were observed by HE staining and Masson staining. TUNEL staining was used to detect cell apoptosis. Immunofluorescence staining was used to assess angiogenesis. Western blotting was used to analyze the expression of ERS-related proteins: Bcl-2, Bax, intracellular apoptotic proteins cleaved Caspase (c-Casp)-3, Casp-12, glucose-regulated protein-78 (GRP-78), and CCAAT/enhancer-binding protein homologous protein (CHOP). Results Compared with the sham group, the MI group rats showed significantly increased LVEDV and LVESV (P<0.05), significantly decreased LVEF and LVFS (P<0.05), disordered myocardial tissue arrangement, significantly increased fibrosis area, increased apoptosis rate, and upregulated expression of ERS-related proteins Bax, c-Casp-3, Casp-12, CHOP, and GRP-78 (P<0.05), while downregulated expression of Bcl-2 (P<0.05). Compared with the MI group, BMSC transplantation improved cardiac function and reduced myocardial injury, with the Cur group showing more significant effects. It further enhanced LVEF and LVFS (P<0.05), downregulated LVEDV and LVESV (P<0.05), and significantly decreased the area of myocardial fibrosis and the rate of apoptosis (P<0.05). The expression of ERS pathway proteins Bax, c-Casp-3, Casp-12, CHOP, and GRP-78 also decreased (P<0.05), while Bcl-2 expression increased significantly (P<0.05). Conclusion Cur pretreatment may enhance the therapeutic effect of BMSC transplantation after myocardial infarction by inhibiting the ERS-mediated apoptosis pathway.

Objective To investigate the expression changes of P-selectin（CD62P）in the doxorubicin （DOX）induced damaged cardiomyocyte line AC16 and atrial myocardial tissue from patients with heart failure(HF). Methods The AC16 cardiomyocyte line was cultured in vitro, and cardiomyocyte injury models with different degrees of damage were established using DOX at concentrations of 1μmol/L, 5μmol/L, and 15μmol/L. The experiment included control group (Ctrl) and myocardial injury model group (IM), which was further divided into mild (IM-Mi), moderate (IM-Mo), and severe (IM-S) subgroups. Immunofluorescence staining (IF) was used to identify the phenotype of AC16 cells, and the CCK-8 assay was employed to detect the proliferative activity of AC16 cells. Western blotting and immunohistochemical (IHC)staining were respectively used to determine the protein expression of CD62P in the AC16 cell line and human HF tissue samples. Additionally, ELISA was conducted to measure the expression levels of CD62P in the supernatant of AC16 cells with different degrees of DOX-induced damage and in the serum of patients with HF. Results In the AC16 cell line, the expression level of CD62P increased with the elevation of DOX concentration （P<0.05）, showing a dose-dependent upward trend. The positive rate of CD62P in the human HF group was significantly higher than that in the control group; Moreover, the expression level of CD62P increased as the severity of HF worsened (P<0.05). The detection result of CD62P in serum were consistent with the expression trend of CD62P in tissue. Conclusion The expression levels of CD62P in local tissues and peripheral serum are positively correlated with the degree of myocardial injury, suggesting that CD62P may serve as a potential biomarker for evaluating the progression of heart failure.

Objective To investigate the adverse effects of superovulatory hormone treatment on the uterus of mice. Methods Twenty-seven female mice were divided into the superovulation recipient group and the normal recipient group (control group, injected with normal saline). For the superovulation recipient group, each mouse was intraperitoneally injected with 7.5 IU pregnant mare serum gonadotropin (PMSG), followed by an injection of 7.5 IU human chorionic gonadotropin (HCG) after 48 hours. All recipients were pseudopregnant mice obtained by cohabitation with vasectomized male mice. In experiment 1, 3.5-day-old blastocysts were transferred into the uteri of recipients in both groups via surgical method, and the implantation rate was subsequently calculated and recorded. In experiment 2, after the blastocysts were transferred into the recipients’ uteri, the embryos were flushed out on 1, 3 and 6 hours post-transfer, respectively, and the morphological changes of the embryos were observed. Omics analysis was performed on the uterine tissue samples collected from normal recipients and superovulation recipients. Results Blastocysts of 3.5 days were separately transferred into the normal and superovulation recipient mice. The embryo implantation rate of the superovulation recipient group was 42.74% on 7.5 days post-transfer, which was significantly lower than that of 74.34% in the normal recipient group (P<0.01). After the embryos were transferred into the uteri of the two recipient groups respectively, the embryos in the uteri of superovulation recipients exhibited varying degrees of damage at different time points, whereas the embryos in the uteri of normal recipients only underwent normal growth and development. For transcriptomic analysis, endometrial tissue samples were collected from recipients on 2.5 days post-treatment, and a total of 1479 differentially expressed genes (DEGs) were identified, including 951 up-regulated genes and 528 down-regulated genes. Among them, 9 significantly up-regulated genes (such as ctla-2α, LCN2 and GPX3) were mainly involved in biological processes including regulation of inflammatory response, oxidative stress and immune effector process. Metabolomic analysis was conducted on uterine tissue samples collected from recipients on 2.5 days post-treatment, and a total of 161 significantly differential metabolites were screened out. Specifically, 55 metabolites were up-regulated and 37 were down-regulated in the positive ion mode, while 53 were up-regulated and 16 were down-regulated in the negative ion mode. Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis indicated that these differential metabolites were mainly enriched in pathways related to metabolic processes. Conclusion After superovulatory hormone treatment, abnormalities in the uterine immune microenvironment and metabolic disorders occur in mice, which impairs the quality of transplanted embryos and thereby reduces the implantation rate.

Objective To update anthropometric records of the Guangxi Yao population, and provide novel data to inform investigations into the ethnic origin of this population. Methods From June to July 2025, the research team conducted a field investigation in Dayao Mountains, Jinxiu Yao Autonomous County, Laibin City, Guangxi Zhuang Autonomous Region. Following the anthropometric method, 31 physical indices and 7 observational indices were analyzed in 150 individuals of the Yao population (76 males and 74 females), and 14 physical indexes were calculated. Data analysis was conducted useing the analysis of variance, u-test, chi-square test, cluster analysis and principal component analysis. Results In the middle-aged Yao population, significant sex differences were detected in 22 indices and 1 index (P<0.05), while R32；Q984in the elderly Yao population, significant sex differences were observed in 22 indices and 3 indexes (P<0.05). In male Yao population, significant age differences were found in 7 indices and 2 indexes between the middle-aged and elderly groups; In female Yao population, significant age differences existed in 13 indices and 5 indexes between the middle-aged and elderly groups. In the overall Yao population, significant sex differences were noted in 3 indexes. According to cephalofacial and body classifications, both males and females in the Yao population were predominantly characterized by brachycephaly, orthocephaly, tapeinocephalic, mesorrhiny, long trunk, mesatiskelic type, wide chest, narrow shoulder, and low stature. Sex differences were observed in the stature-crista iliaca index and morphological facial index; males mainly presented medium crista iliaca and mesoprosopy, whereas females mainly exhibited wide crista iliaca and leptoprosopy. Conclusion The Yao population in Dayao mountain exhibits southern-type anthropological characteristics and may share closer affinity with the Guangxi Miao, Guangxi Dong, and Guizhou Shui populations based on head facial and body characteristics.

Objective To conduct a detailed anatomical investigation of the first metatarsophalangeal joint (MTP1) capsule-ligament complex and perform three-dimensional(3D) digital reconstruction based on these findings, providing intuitive and stereoscopic morphological evidence for the clinical diagnosis, surgical planning, and treatment of hallux valgus. Methods Six adult foot specimens fixed in 4% formaldehyde were selected. A step-by-step dissection method from superficial to deep layers was employed, using microsurgical instruments for meticulous separation. The morphology, attachment points, and adjacent relationships of the joint capsule, collateral ligament system, plantar plate, deep transverse metatarsal ligament, and surrounding tendons were preserved intact. Based on the spatial data obtained from the dissection, a high-precision digital reconstruction of the bones and 10 major ligaments was performed using 3D modeling software (Blender 4.5), achieving structural visualization through differential rendering. Results A microanatomical specimen of the capsule ligament complex around MTP1 was successfully produced, which clearly displayed the morphology, course, and spatial position relationship of each structure. Multi view three-dimensional anatomical images of the 10 main ligaments around MTP1 were produced, and the structural characteristics and spatial position relationship of each ligament were clearly displayed through visual enhancement technology. A 3D digital image of the microscopic and complex ligament system of MTP1 was reconstructed. Conclusion The microanatomical specimens of the capsule ligament complex produced in this study provide anatomical basis for the diagnosis and treatment of eversion. The constructed 3D digital model not only deepens the understanding of the three-dimensional spatial structure of the complex, but also enhances its generalizability and has the potential to be transformed into 3D printing and surgical simulation.

Objective To establish primary culture，expansion，and identification methods for rat inferior vena cava (IVC)-derived mesenechymal stem cells(MSCs)，providing a novel alternative source. Methods Rat IVC-MSCs were isolated using mechanical fragmentation combined with enzymatic digestion. Multidimensional characterization included morphological observation，flow cytometry for surface immunophenotyping，and trilineage differentiation (osteogenic，adipogenic and chondrogenic) induction with histological staining. Results Primary cells exhibited short spindle morphology with adherent growth and robust proliferation. At passage 4，marker protein expression: CD90 （97.57 ± 2.83）%、CD73 （99.67 ± 0.06）%、CD44 （99.53 ± 0.06）%，positive rate of positive markers > 95%；CD45 （3.24 ± 0.19）%、CD34 （3.82 ± 0.31）%、CD11b/c （4.88 ± 0.24）%，positive rate of negative markers <5%. Induced cells successfully differentiated into osteoblasts，adipocytes，and chondrocytes，demonstrating multipotency. Conclusion We successfully established a rat IVC-MSC culture system，expanding the MSC“seed bank” to this uncommon source. This broadens MSC acquisition avenues and establishes a reproducible platform for investigating biological characteristics, elucidating venous homeostasis mechanisms, and developing stem cell therapies for vascular diseases，providing a paradigm for clinical translation of stem cells from rare tissue sources.

Depressive disorder is a mental disorder with complex etiology and pathogenesis. The neurotrophic hypothesis has recently garnered significant attention. Brain-derived neurotrophic factor (BDNF) is crucial for the central nervous system (CNS). They specifically bind to the tyrosine kinase receptor B (TrkB), activating its downstream signaling pathways. Hesperidin, a flavonoid compound, exhibits a range of biological effects, including antioxidant, anti-inflammatory, anticancer, neuroprotective, and antidepressant properties. Interestingly, hesperidin can activate and upregulate BDNF levels, which plays a significant role in anti-inflammation, antioxidation, neuronal survival, and synaptic plasticity. This review explores the antidepressant efficacy of hesperidin, highlighting its role in mitigating depressive symptoms through the activation of critical molecular pathways such as BDNF/TrkB signaling, nuclear factor-kappa B (NF-κB), the hypothalamic-pituitary-adrenal (HPA) axis, and monoamine oxidase A/B (MAO-A/MAO-B). Clearly, the multifaceted antidepressant effects and favorable safety profile of hesperidin highlight its significant potential in the field of natural therapeutic agents.