南方医科大学学报杂志最新文献

{"title":"[<i>In vitro</i> culture, expansion, and biological characterization of mesenchymal stem cells derived from neonatal rat liver].","authors":"Ming Chi, Boling Li, Jing Wu, Jianyun Ge, Yuanyu Tang","doi":"10.12122/j.issn.1673-4254.2026.04.20","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.20","url":null,"abstract":"<p><strong>Objectives: </strong>To isolate liver-derived mesenchymal stem cells (L-MSCs) from neonatal rats using tissue explant method combined with enzymatic digestion.</p><p><strong>Methods: </strong>Liver tissues aseptically harvested from 1-week-old SD rats were rinsed, minced, and digested with D-Hanks solution containing 0.1% type-II collagenase and 0.05% type-IV collagenase for 15-20 min. After filtration through a 100-mesh screen, the cells were cultured for primary L-MSC isolation. The target cells were identified by morphological observation, flow cytometric analysis of surface CD markers, and adipogenic/osteogenic differentiation assays.</p><p><strong>Results: </strong>Six to eight days after primary seeding, short spindle-shaped adherent cells formed a confluent monolayer arranged in a swirling pattern. Flow cytometry of passage-4 cells showed high expressions of CD90 [(99.33±0.06)%], CD73 [(99.60±0.10)%], CD44 [(99.50±0.10)%], and CD29 [(97.60±0.17)%] with an average positive rate of (99.01±0.86)% and low expressions of CD45 [(0.87±0.12)%], CD34 [(0.95±0.22)%], and CD11b/c [(1.71±0.28)%] with an average positive rate of (1.18±0.44)%, which was significantly lower than that of CD90, CD73, CD44, and CD29 (<i>P</i><0.01), consistent with the immunophenotypic characteristics of MSCs. Both adipogenic and osteogenic induction tests of the cells yielded positive results.</p><p><strong>Conclusions: </strong>L-MSCs can be successfully isolated from neonatal rat liver using tissue explant method combined with enzymatic digestion.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"923-928"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[<i>Jia Wei Qingxin</i> Lotus Seed Drink improves diabetic kidney disease in mice by regulating the KDM3C/SP1 signaling pathway].","authors":"Jiarun Xie, Yanyu Luo, Jinjin Xia, Ming Wang","doi":"10.12122/j.issn.1673-4254.2026.04.02","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.02","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the therapeutic effect of <i>Jia Wei Qingxin</i> Lotus Seed Drink (QISD) on renal injury in mice with diabetic kidney disease (DKD) and its mechanism.</p><p><strong>Methods: </strong>The immunogenes differentially expressed in renal tubular epithelial cells (HK-2) induced by late glycosylation end products were screened using GSE193192 dataset from GEO database and the pharmacological mechanisms were predicted. Male ICR mouse models of DKD established by high-fat feeding for 4 weeks and intraperitoneal streptozotocin injection for 5 days were randomized for treatment with low (14.46 g/kg), medium (28.92 g/kg) and high (57.84 g/kg) doses of QISD via gavage for 12 weeks, with dapagliflozin as the positive control drug (<i>n</i>=8). Penal pathologies of the mice were observed by HE, PAS and Masson staining, and renal expression levels of KDM3C, SP1, TNF-α, and MCP-1 mRNAs and proteins were detected using RT-qPCR and Western blotting. In a HK-2 cell model of lipopolysaccharide (LPS)-induced inflammatory injury, the effects of small-molecule inhibitors were tested to explore the therapeutic mechanism of QISD against cell inflammation.</p><p><strong>Results: </strong>QISD treatment significantly lowered serum levels of glycated serum protein, creatinine and urea nitrogen, reduced glycogen accumulation, attenuated glomerular hypertrophy, and decreased renal inflammatory infiltration in DKD mouse models. QISD also reduces the expression levels of KDM3C, SP1, TNF‑α and MCP-1 in the kidney tissues of the mice. In LPS-induced HK-2 cells, the application of JIB-04, an inhibitor of KDM3C, obviously suppressed the expression levels of the inflammatory factors including TNF‑α, MCP-1 and ICAM-1.</p><p><strong>Conclusions: </strong>QISD can ameliorate renal injury in DKD mice by inhibiting inflammatory response <i>via</i> suppressing excessive activation of the KDM3C/SP1 signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"728-741"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Electroacupuncture at Baihui and Zusanli improves fear memory extinction in single prolonged stress mice by activating hippocampal astrocytes].","authors":"Xiaoyu Chen, Chang Liu, Shaojie Yang, Juan Wang, Ping Cheng, Hongyu Yin, Jingji Wang, Guoqi Zhu","doi":"10.12122/j.issn.1673-4254.2026.04.18","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.18","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the effect of electroacupuncture (EA) on fear memory extinction in single prolonged stress (SPS) mice and the potential mechanism involving astrocytes.</p><p><strong>Methods: </strong>Thirty-six male C57BL/6J mice were randomly divided into the control, SPS model, EA treatment, paroxetine positive drug (PRX), Saline and CNO group. In Saline and CNO group, chemical genetic virus was used to inhibit the hippocampal astrocytes. Except for control group, the other groups were subjected to SPS modeling. After 7 days, the EA, Saline and CNO group were treated with EA at Baihui and Zusanli, while PRX group was given paroxetine solution for 10 days. Fear conditioning test and elevated plus maze test were used to evaluate fear memory extinction and anxiety-like behaviors, and the CNO group was administered CNO 30 minutes before the tests start. Immunofluorescence staining was used to observe the changes in the number and morphology of hippocampal astrocytes, and hippocampal expressions of GFAP and CX43 proteins were detected using Western blotting.</p><p><strong>Results: </strong>In the mouse models with SPS, EA intervention significantly reduced the freezing time during fear re-exposure for 3-15 min and in the fear extinction phase. EA intervention also significantly increased the extinction coefficient, time spent in the open arms, the mean fluorescence intensity of GFAP, the number of astrocyte branches 50 μm from the soma, and the expression of CX43 proteins in the hippocampus of SPS mice.</p><p><strong>Conclusions: </strong>EA at Baihui and Zusanli improves fear memory extinction and anxiety-like behaviors in SPS mice by activating hippocampal astrocytes.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"899-906"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-24-3p promotes spinal cord injury repair in rats by inhibiting ferroptosis <i>via</i> targeting GSK-3β.","authors":"Dongmin Wei, Bingbing Wang, Jianzhong Gao, Tianyu Zhai, Xinyue Bai, Jinghui Zhu, Can Zhang, Caizhen Shi, Qin Hao, Chen Chen, Lin Zhao","doi":"10.12122/j.issn.1673-4254.2026.04.01","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.01","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the molecular mechanism by which miR-24-3p promotes spinal cord injury (SCI) repair in rats.</p><p><strong>Methods: </strong>The changes in spinal cord miR-24-3p expression was detected in a SD rat model of SCI with qRT-PCR. Using a stereotaxic apparatus, miR-24-3p agomir or a negative control reagent was microinjected at 3 mm rostral and caudal to the SCI epicenter of the rats<i>.</i> Motor function recovery of the SCI rats was evaluated with BBB scores, histopathological changes and Fe²⁺ content in the SCI area were examined with HE staining and a commercial assay kit, and the changes in iron deposition in the SCI area was observed using Prussian blue staining with DAB. Western blotting and immunofluorescence staining were used to detect expressions of glycogen synthase kinase-3β (GSK-3β) and ferroptosis-related proteins xCT and GPX4 in the injured tissue. The targeted regulatory relationship between miR-24-3p and GSK-3β was verified using dual-luciferase reporter assay. In PC12 cells with erastin-induced ferroptosis, malondialdehyde (MDA) content was detected and the expression levels of GSK-3β, xCT and GPX4 proteins were determined by Western blotting and immunofluorescence staining.</p><p><strong>Results: </strong>The expression of miR-24-3p and protein levels of xCT and GPX4 were significantly decreased in the SCI area of the rat models. Treatment with miR-24-3p agomir significantly improved hindlimb motor function of the SCI rats, alleviated spinal cord pathologies, reduced Fe²⁺ content, iron deposition and GSK-3β protein expression, and upregulated xCT and GPX4 protein expressions in the SCI area. Dual-luciferase reporter assay confirmed targeted inhibition of GSK-3β by miR-24-3p. In erastin-induced PC12 cells, transfection with miR-24-3p mimics significantly decreased intracellular MDA content and GSK-3β protein expression and increased xCT and GPX4 protein levels, and these effects were enhanced by co-transfection with GSK-3β inhibitor.</p><p><strong>Conclusions: </strong>miR-24-3p promotes repair of SCI in rats by inhibiting ferroptosis via targeted suppression of GSK-3β.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"715-727"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[<i>Jintiange</i> Capsule alleviates glucocorticoid-induced osteoporosis in rats by inhibiting vascular endothelial cell senescence and promoting bone formation].","authors":"Zihao Deng, Zhuan Wang, Senxiong Meng, Yusheng Yang, Yunping Yang, Liuyi Fan, Lei Wang","doi":"10.12122/j.issn.1673-4254.2026.04.14","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.14","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of cellular senescence in glucocorticoid-induced osteoporosis and explore the therapeutic mechanism of <i>Jintiange</i> (JTG) Capsule.</p><p><strong>Methods: </strong>Cultured human umbilical vein endothelial cells (HUVECs) and mouse pre-osteoblasts (MC3T3) were treated with methylprednisolone (MPS) or MPS combined with JTG Capsule dissolved in saline. HUVEC senescence pathways and repair capacity were analyzed using Western blotting, SA-β-Gal staining, DCFH-DA assay, scratch wound healing, and RT-PCR. The osteogenic potential of MC3T3 cells was assessed using immunofluorescence staining, ALP staining, Alizarin Red S staining, and RT-PCR. Osteoclast differentiation was evaluated by TRAP staining. Thirty 3-week-old female SD rats were randomized into control, MPS, and MPS+JTG groups, and the rats in the latter two groups received daily intraperitoneal MPS injections and treated with gavage of saline or JTG Capsule suspension for 3 months. Femurs and venous blood were collected from the rats for micro-CT analysis of femoral bone volume fraction and detection of serum bone metabolism markers.</p><p><strong>Results: </strong>Network pharmacology revealed that the active components of tiger bone had numerous intersection targets with glucocorticoid-induced osteoporosis with a strong binding affinity to cellular senescence-related targets such as P53. In MPS-treated HUVEC-derived osteoclasts, treatment with JTG Capsule significantly inhibited the expressions of P53 and P21, attenuated oxidative stress, and enhanced cell migration and angiogenic capacity. Similarly, JTG Capsule significantly enhanced osteogenic and mineralization capacities of MC3T3 cells and suppressed osteoclast differentiation. In the rat models, intraperitoneal MPS injection for 14 days resulted in significant bone loss in the femur, and JTG Capsule treatment obviously alleviated bone loss and ameliorated the disorder in serum bone metabolic markers.</p><p><strong>Conclusions: </strong>JTG Capsule alleviates MPS-induced HUVEC senescence, enhances osteogenic capacity and suppresses osteoclastogenesis in MC3T3 cells, and promotes intraosseous angiogenesis to improve glucocorticoid-induced osteogenesis inrats.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"861-870"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Dynamic changes and physiological regulation of common carotid artery blood flow during general anesthesia in elderly patients: a prospective study].","authors":"Xingyang Liu, Jinghan Wu, Chunyan Ye, E Wang, Hao Hu","doi":"10.12122/j.issn.1673-4254.2026.04.05","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.05","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the dynamic pattern and physiological regulation of common carotid artery (CCA) blood flow during general anesthesia in elderly patients.</p><p><strong>Methods: </strong>A total of 193 elderly patients undergoing abdominal surgery were prospectively enrolled. Respiratory and hemodynamic variables and anesthetic depth of the patients were recorded throughout the perioperative period. CCA blood flow was measured at predefined time points using vector flow imaging. Heart rate, mean arterial pressure, end-tidal carbon dioxide, and bispectral index were included in a linear mixed-effects model, with patient ID as a random effect, to explore the physiological determinants of intraoperative CCA blood flow.</p><p><strong>Results: </strong>CCA blood flow showed clear stage-related changes during general anesthesia. The mixed-effects model explained 52.0% of the variation in CCA blood flow (adjusted <i>R</i>²=0.520, <i>P</i><0.001). Heart rate, mean arterial pressure, end-tidal carbon dioxide, and bispectral index were all significantly associated with CCA blood flow (all <i>P</i><0.001). The standardized model further showed that the strength of these associations differed, with flow-related factors showing a stronger effect than blood pressure or heart rate alone. Surgical approach and patient position had no significant effect on CCA blood flow.</p><p><strong>Conclusions: </strong>Intraoperative cerebral perfusion is not maintained by blood pressure alone but influenced jointly by ventilation, hemodynamic status, and anesthetic depth. Recognizing and managing these factors may help optimize cerebral perfusion during surgery.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"761-769"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Overexpression of miR-593-5p inhibits migration, invasion and proliferation and promotes apoptosis of gastric cancer cells by targeting PLK1].","authors":"Baolong Dong, Jiangshan Peng, Jinru Li, Yun Meng, Xiaojun Yang","doi":"10.12122/j.issn.1673-4254.2026.04.15","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.15","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the role of miR-593-5p targeting Polo-like kinase 1 (PLK1) in regulating biological behaviors of human gastric cancer (GC) cells.</p><p><strong>Methods: </strong>Four GC cell lines (MGC-803, AGS, HGC-27, and MKN-45) and normal human gastric mucosal epithelial GES-1 cells were examined for miR-593-5p and PLK1 expressions using RT-PCR, and MGC-803 cells with the lowest miR-593-5p expression and MKN-45 with highest miR-593-5p expression were selected for subsequent experiments. TargetScan7.2 was used to predict the binding between miR-593-5p and PLK1. MGC-803 cells were transfected with miR-593-5p mimic or mimic NC via liposome, and MKN-45 cells were transfected with miR-593-5p inhibitor or inhibitor NC. The changes in cellular PLK1 protein expression levels were detected using Western blotting, and the changes in biological behaviors of the cells were evaluated using scratch assay, Transwell assay, CCK-8 assay, and flow cytometry.</p><p><strong>Results: </strong>Compared with GES-1 cells, the GC cell lines showed significantly downregulated miR-593-5p and upregulated PLK1 expressions. TargetScan7.2 identified binding sites between miR-593-5p and PLK1 3'UTR. In MGC-803 cells, miR-593-5p overexpression caused significant reduction of PLK1 protein expression, inhibited cell migration, invasion, and proliferation, and promoted cell apoptosis. Conversely, miR-593-5p inhibition in MKN-45 cells upregulated PLK1 expression, enhanced cell migration, invasion, and proliferation, reduced cell apoptosis.</p><p><strong>Conclusions: </strong>miR-593-5p overexpression inhibits GC cell migration, invasion, and proliferation, and promotes apoptosis, likely by directly downregulating PLK1, suggesting the role of miR-593-5p as a tumor suppressor in GC and its potential therapeutic relevance.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"871-879"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Long non-coding RNA LASTR promotes progression of head and neck squamous cell carcinoma by binding to miR-4476 and upregulating BCAM expression].","authors":"Bo Wu, Ru Song, Ning Gao, Keyao Xing, Penghui Zhang, Moyi Qu, Huimin Zhang","doi":"10.12122/j.issn.1673-4254.2026.04.03","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.03","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the regulatory role and mechanism of long non-coding RNA LASTR in progression of head and neck squamous cell carcinoma (HNSCC).</p><p><strong>Methods: </strong>LASTR expression in HNSCC and its correlation with patient prognosis were analyzed using TCGA and GEO transcriptomic data, and its expression in HNSCC cell lines was validated by qPCR. In a loss-of-function HNSCC cell model with siRNA-mediated LASTR knockdown, the changes in cell proliferation, migration, and invasion were assessed by high-content counting, CCK-8 assay, ATP detection, and Transwell assay. Bioinformatic analysis was conducted to identify the target genes of LASTR, and their interactions with BCAM were verified by qPCR and immunoblotting. The LASTR-miR-4476-BCAM regulatory axis was confirmed with RNA pulldown and dual-luciferase assays. The functional role of BCAM was investigated, and rescue experiments were performed to determine if BCAM mediates the effects of LASTR expression modulation.</p><p><strong>Results: </strong>LASTR was significantly upregulated in HNSCC tissues and cell lines, and its high expression was significantly correlated with poor patient prognosis. In HNSCC cells, LASTR knockdown significantly suppressed cell proliferation, migration, and invasion. Bioinformatic analysis revealed 78 candidate target genes of LASTR, enriched in pathways involving angiogenesis, hypoxia response, MAPK, ErbB, and Ras signaling. LASTR knockdown obviously decreased BCAM expression HNSCC cells. Mechanistically, LASTR upregulated BCAM by sequestering miR-4476. BCAM knockdown similarly suppressed malignant phenotypes of HNSCC cells, and its overexpression rescued the inhibitory effects of LASTR knockdown.</p><p><strong>Conclusions: </strong>LASTR is upregulated in HNSCC and associated with poor prognosis. High expression of LASTR promotes HNSCC progression by acting as a ceRNA for miR-4476 to upregulate BCAM, suggesting the role of LASTR and BCAM as potential biomarkers and therapeutic targets for HNSCC.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"742-752"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[<i>Zhizichi</i> Decoction alleviates depression-like behaviors in rats exposed to chronic unpredictable mild stress by modulating tryptophan metabolism and the BDNF signaling pathway].","authors":"Tuo Meng, Mingjun Qin, Yonggang Xia","doi":"10.12122/j.issn.1673-4254.2026.04.17","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.17","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the regulatory effects of <i>Zhizichi</i> Decoction on tryptophan metabolism, inflammation, and neurotrophic factor-related signaling pathways and its potential antidepressant effects in a rat model of depression induced by chronic unpredictable mild stress (CUMS).</p><p><strong>Methods: </strong>Adult male SD rat models of CUMS-induced depression were randomized into CUMS model group, fluoxetine group, low-dose <i>Zhizichi</i> Decoction group (LZZCD), and high-dose <i>Zhizichi</i> Decoction group (HZZCD) (<i>n</i>=10), with another 10 normal rats as the control group. After modeling, the rats received daily drug interventions via gavage for 4 weeks. Forced swimming test, tail suspension test, and voluntary activity recording were used to assess depressive-like behaviors of the rats. HE staining, Western blotting and ELISA were used to evaluate the changes in brain tissue pathologies, tryptophan metabolism, neurotransmitter levels, inflammation and brain-derived neurotrophic factor (BDNF)-related pathways of the rats.</p><p><strong>Results: </strong>The rat models with CUMS showed significantly increased immobility and reduced swimming and struggling time. Both fluoxetine and <i>Zhizichi</i> Decoction at the two doses markedly alleviated depressive-like behaviors of the rat models, and high-dose <i>Zhizichi</i> Decoction produced the strongest ameliorating effect. <i>Zhizichi</i> Decoction treatment reduced brain injury scores of the rats, upregulated TPH2 and downregulated IDO, KMO, and MAO-A expressions in the hippocampus, causing also inhibition of the NF‑κB/NLRP3 pathway and increased hippocampal expressions of TrkB, p-CREB, p-AKT, and p-ERK. ELISA results demonstrated that <i>Zhizichi</i> Decoction treatment increased Trp, 5-HT, and 5-HIAA levels, decreased the levels of Kyn and inflammatory cytokines, and upregulated BDNF expression in the hippocampus of the rat models.</p><p><strong>Conclusions: </strong><i>Zhizichi</i> Decoction alleviates depressive-like behaviors and brain pathologies in CUMS rats by regulating tryptophan metabolism, enhancing synthesis and reducing degradation of neurotransmitters, inhibiting inflammatory response, and upregulating the BDNF signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"890-898"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress in mechanisms of dietary resistant starch for regulating glucose and lipid metabolism].","authors":"Kun Liu, Xiaoying Li, Yugang Zhang, Jia Sun, Wenzhen Liao","doi":"10.12122/j.issn.1673-4254.2026.04.24","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.24","url":null,"abstract":"<p><p>The global prevalence of metabolic diseases such as obesity, diabetes, and cardiovascular diseases is closely related to overnutrition and imbalanced dietary patterns. As an important carbohydrate, starch directly affects the homeostasis of glucose and lipid metabolism due to its digestion characteristics. Resistant starch (RS) with unique anti-digestive properties and prebiotic functions has become the current hotspot in dietary nutrition research for improving glucose and lipid metabolism disorders. This review summarizes the digestive characteristics of starch and the comprehensive effects of RS and its mechanisms for ameliorating metabolic diseases. Diets with high RS content not only optimize glucose homeostasis by delaying glucose release, the undigested fractions entering the colon also drive the metabolic regulatory network of the gut microbiota-gut-brain axis by activating the AMPK/ACC pathway to reduce fat accumulation, enhancing intestinal barrier function mediated by short-chain fatty acids (SCFAs), and promoting GLP-1/PYY neural signal transduction. These insights facilitate the design of new healthy foods and inspire new strategies for optimizing dietary nutrition and regulating glucose and lipid metabolism disorders caused by high-carbohydrate diets.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"956-966"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}