南方医科大学学报杂志最新文献

{"title":"[Monotropein improves motor function of mice with spinal cord injury by inhibiting the PI3K/AKT signaling pathway to suppress neuronal apoptosis].","authors":"Yue Chen, Linyu Xiao, Lü Ren, Xue Song, Jing Li, Jianguo Hu","doi":"10.12122/j.issn.1673-4254.2025.04.13","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.13","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effect of monotropein on motor function recovery of mice with spinal cord injury (SCI) and explore the underlying mechanism.</p><p><strong>Methods: </strong>Forty-five adult female C57BL/6 mice were randomized equally into sham operation group, SCI group, and SCI group with daily intraperitoneal monotropein injection. The mice in the former two groups received daily saline injections. Motor function of the mice was evaluated using BMS scores, slant plate test, and footprint analyses. Pathological changes and neuronal counts in the spinal cord were observed using HE, LFB, and Nissl staining. The biological functions of monotropein were explored using GO and KEGG enrichment analyses. NeuN/cleaved caspase-3 immunofluorescence assay and Western blotting were used to detect neuronal apoptosis in the spinal cord of the mice. In cultured HT22 cells, the effect of monotropein on TNF-α-induced cell apoptosis was evaluated using TUNEL staining and Western blotting. In monotropein-treated HT22 cells and SCI mice, the changes in the PI3K/AKT pathway were examined, and the effect of a PI3K/AKT pathway activator (IGF-1) on HT22 cell apoptosis and motor function recovery of SCI mice were observed.</p><p><strong>Results: </strong>SCI mice with monotropein treatment showed significantly improved motor functions with reduced SCI areas and increased myelin retention and neuron counts in the spinal cord. Bioinformatics analysis suggested a role of PI3K/AKT signaling pathway in mediating the anti-apoptotic effects of monotropein. In SCI mice, monotropein obviously reduced apoptotic neurons, decreased expressions of cleaved caspase-3 and Bax and increased Bcl-2 expression in the spinal cord. In HT22 cells, monotropein significantly inhibited TNF-α-induced apoptosis and PI3K/AKT pathway activation. Treatment with IGF-1 obviously increased apoptosis of HT22 cells and exacerbated locomotor dysfunction in SCI mice.</p><p><strong>Conclusions: </strong>Monotropein promotes motor function recovery in SCI mice by reducing neuronal apoptosis possibly by inhibiting the PI3K/AKT signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"774-784"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144026217","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":"[Changes in circulating levels of calcium and bone metabolism biochemical markers in patients receiving denosumab treatment].","authors":"Yuancheng Chen, Wen Wu, Ling Xu, Haiou Deng, Ruixue Wang, Qianwen Huang, Liping Xuan, Xueying Chen, Ximei Zhi","doi":"10.12122/j.issn.1673-4254.2025.04.11","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.11","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the changes in blood levels of calcium and bone metabolism biochemical markers in patients with primary osteoporosis receiving treatment with denosumab.</p><p><strong>Methods: </strong>Seventy-three patients with primary osteoporosis treated in our Department between December, 2021 and December 2023 were enrolled. All the patients were treated with calcium supplements, vitamin D and calcitriol in addition to regular denosumab treatment every 6 months. Blood calcium, parathyroid hormone (PTH), osteocalcin (OC), type I procollagen amino-terminal propeptide (PINP), and type I collagen carboxy-terminal telopeptide β special sequence (β‑CTX) data before and at 3, 6, 9, and 12 months after the first treatment were collected from each patient.</p><p><strong>Results: </strong>Three months after the first denosumab treatment, the bone turnover markers (BTMs) OC, PINP, and β-CTX were significantly decreased compared to their baseline levels by 39.5% (<i>P</i><0.001), 56.2% (<i>P</i><0.001), and 81.8% (<i>P</i><0.001), respectively. At 6, 9, and 12 months of treatment, OC, PINP, and β-CTX remained significantly lower than their baseline levels (<i>P</i><0.001). Blood calcium level was decreased (<i>P</i><0.05) and PTH level increased (<i>P</i><0.05) significantly in these patients at months of denosumab treatment, but their levels were comparable to the baseline levels at 6, 9, and 12 months of the treatment (<i>P</i>>0.05).</p><p><strong>Conclusions: </strong>Denosumab can suppress BTMs and has a good therapeutic effect in patients with primary osteoporosis, but reduction of blood calcium and elevation of PTH levels can occur during the first 3 months in spite of calcium supplementation. Blood calcium and PTH levels can recover the baseline levels as the treatment extended, suggesting the importance of monitoring blood calcium and PTH levels during denosumab treatment.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"760-764"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036324","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>Zheng Gan</i> Decoction inhibits diethylnitrosamine-induced hepatocellular carcinoma in rats by activating the Hippo/YAP signaling pathway].","authors":"Tianli Song, Yimin Wang, Tong Sun, Xu Liu, Sheng Huang, Yun Ran","doi":"10.12122/j.issn.1673-4254.2025.04.15","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.15","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the inhibitory effect of <i>Zheng Gan</i><i>Decoction</i> (ZGF) on tumor progression in a rat model of diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) and explore the possible mechanism.</p><p><strong>Methods: </strong>Seventy SD rats were subjected to regular intraperitoneal injections of DEN (50 mg/kg) for 12 weeks to induce HCC tumorigenesis, with another 10 rats receiving saline injections as the normal control. After successful modeling, the rats were randomized into 5 groups (<i>n</i>=10) for daily treatment with distilled water ( model group), <i>Huaier</i> Granules (4 g/kg; positive control group), or ZGF at low, medium, and high doses (2, 4, and 8 g/kg, respectively) via gavage for 17 weeks. Body weight changes of the rats were monitored, and after completion of the treatments, the rats were euthanized for measurement of liver, spleen and thymus indices and morphological and histopathological examinations of the liver tissues using HE staining. The expressions of YAP, p-YAP, MST1, LATS1 and p-LATS1 in the liver tissues were detected using immunohistochemistry and Western blotting.</p><p><strong>Results: </strong>Compared with the normal control rats, the rat models with DEN-induced HCC exhibited much poorer general condition with a significantly reduced survival rate, increased body weight and liver and spleen indices, and a lowered thymus index. ZGF treatment obviously reduced liver and spleen indices, increased the thymus index, and improved pathologies of the liver tissues of the rat models. Immunohistochemistry and Western blotting showed a dose-dependent reduction of YAP expression and an increment of p-YAP expression in ZGF-treated rats, which also exhibited significantly upregulated hepatic expressions of MST1, LATS1 and p-LATS1.</p><p><strong>Conclusions: </strong>ZGF inhibits DEN-induced HCC in rats by activating the Hippo/YAP pathway <i>via</i> upregulating MST1 and LATS1 expression, which promotes YAP phosphorylation and degradation to suppress proliferation and induce apoptosis of the tumor cells.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"799-809"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045331","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":"[Amentoflavone alleviates acute lung injury in mice by inhibiting cell pyroptosis].","authors":"Yalei Sun, Meng Luo, Changsheng Guo, Jing Gao, Kaiqi Su, Lidian Chen, Xiaodong Feng","doi":"10.12122/j.issn.1673-4254.2025.04.03","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.03","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effect of amentoflavone (AF) for alleviating lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and inhibiting NLRP3/ASC/Caspase-1 axis-mediated pyroptosis.</p><p><strong>Methods: </strong>Female BALB/c mice were randomly divided into control group, LPS group, and AF treatment groups at low, moderate and high doses (<i>n</i>=12<i>)</i>. ALI models were established by tracheal LPS instillation, and in AF treatment groups, AF was administered by gavage 30 min before LPS instillation. Six hours after LPS instillation, the mice were euthanized for examining lung tissue histopathological changes, protein levels in BALF, and MPO levels in the lung tissue. In the <i>in vitro</i> experiment, RAW264.7 cells were pretreated with AF, AC (a pyroptosis inhibitor), or their combination for 2 h before stimulation with LPS and ATP. The changes in cell proliferation and viability were detected using CCK-8 assay, and IL-1β, IL-6, IL-18, and TNF-α levels were determined with ELISA. Immunohistochemistry, immunofluorescence assay, and immunoblotting were used to detect the protein levels of NLRP3, ASC, cleaved caspase-1, and GSDMD N in rat lung tissues and the treated cells.</p><p><strong>Results: </strong>In mice with LPS exposure, AF treatment significantly improved lung pathologies and edema, reduced protein levels in BALF and pulmonary MPO level, inhibited the high expression of NLRP3/ASC/Aspase-1 axis, reduced the expression of GSDMD N, and lowered the release of IL-1β, IL-6, IL-18, and TNF‑α. In RAW264.7 cells with LPS and ATP stimulation, AF pretreatment effectively reduced cell death, inhibited activation of the NLRP3/ASC/Aspase-1 axis, and reduced GSDMD N expression and the inflammatory factors. The pyroptosis inhibitor showed a similar effect to AF, and their combination produced more pronounced effects in RAW264.7 cells.</p><p><strong>Conclusions: </strong>Amentoflavone can alleviate ALI in mice possibly by inhibiting NLRP3/ASC/Caspase-1 axis-mediated cell pyroptosis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"692-701"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033099","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":"[Construction of recognition models for subthreshold depression based on multiple machine learning algorithms and vocal emotional characteristics].","authors":"Meimei Chen, Yang Wang, Huangwei Lei, Fei Zhang, Ruina Huang, Zhaoyang Yang","doi":"10.12122/j.issn.1673-4254.2025.04.05","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.05","url":null,"abstract":"<p><strong>Objectives: </strong>To construct vocal recognition classification models using 6 machine learning algorithms and vocal emotional characteristics of individuals with subthreshold depression to facilitate early identification of subthreshold depression.</p><p><strong>Methods: </strong>We collected voice data from both normal individuals and participants with subthreshold depression by asking them to read specifically chosen words and texts. From each voice sample, 384-dimensional vocal emotional feature variables were extracted, including energy feature, Meir frequency cepstrum coefficient, zero cross rate feature, sound probability feature, fundamental frequency feature, difference feature. The Recursive Feature Elimination (RFE) method was employed to select voice feature variables. Classification models were then built using the machine learning algorithms Adaptive Boosting (AdaBoost), Random Forest (RF), Linear Discriminant Analysis (LDA), Logistic Regression (LR), Lasso Regression (LRLasso), and Support Vector Machine (SVM), and the performance of these models was evaluated. To assess generalization capability of the models, we used real-world speech data to evaluate the best speech recognition classification model.</p><p><strong>Results: </strong>The AdaBoost, RF, and LDA models achieved high prediction accuracies of 100%, 100%, and 93.3% on word-reading speech test set, respectively. In the text-reading speech test set, the accuracies of the AdaBoost, RF, and LDA models were 90%, 80%, and 90%, respectively, while the accuracies of the other 3 models were all below 80%. On real-world word-reading and text-reading speech data, the classification models using AdaBoost and Random Forest still achieved high predictive accuracies (91.7% and 80.6% for AdaBoost and 86.1% and 77.8% for Random, respectively).</p><p><strong>Conclusions: </strong>Analyzing vocal emotional characteristics allows effective identification of individuals with subthreshold depression. The AdaBoost and RF models show excellent performance for classifying subthreshold depression individuals, and may thus potentially offer valuable assistance in the clinical and research settings.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"711-717"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972398","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":"[Effects of liver fibrosis induced by iron overload on M2 polarization of macrophages in mice].","authors":"Jiawen Yu, Yi Zhou, Chunmei Qian, Lan Mu, Renye Que","doi":"10.12122/j.issn.1673-4254.2025.04.02","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.02","url":null,"abstract":"<p><strong>Objectives: </strong>To observe the evolution of intrahepatic macrophage polarization in mice with liver fibrosis induced by iron overload.</p><p><strong>Methods: </strong>Thirty-two C57BL/6 mice (6-8 weeks) were randomized into control group (<i>n</i>=8) and liver fibrosis model group (<i>n</i>=24) induced by aidly intraperitoneal injection of iron dextran. At the 3rd, 5th, and 7th weeks of modeling, 8 mice in the model group were sacrificed for observing liver fibrosis using Masson, Sirius Red and immunohistochemical staining and detecting serum levels of ALT, AST and the levels of serum iron, ferritin, liver total Fe and ferrous Fe. iNOS⁺/F4/80⁺ cells and CD206⁺/F4/80⁺ cells were detected by double immunofluorescence assay to observe the proportion and distribution of M1 and M2 macrophages. The hepatic expressions of Arg-1, iNOS, IL-6, IL-10, and TNF‑α proteins were detected using Western blotting or ELISA, and the expression of CD206 mRNA was detected using RT-PCR.</p><p><strong>Results: </strong>The mice in the model group showed gradual increase of fibrous tissue hyperplasia in the portal area over time, structural destruction of the hepatic lobules and formation of pseudolobules. With the passage of time during modeling, the rat models showed significantly increased hepatic expressions of α-SMA and COL-1, elevated serum levels of ALT, AST, Fe, ferritin, and increased liver total Fe and ferrous Fe levels. The expressions of M1 polarization markers IL-6, TNF‑α, and iNOS all increased with time and reached their peak levels at the 3rd week; The expressions of M2 polarization markers (IL-10 and Arg-1 proteins and CD206 mRNA) significantly increased in the 3rd week and but decreased in the 5th and 7th weeks.</p><p><strong>Conclusions: </strong>Iron overload promotes M1 polarization of macrophages in mice. Liver fibrosis in the early stage promotes M2 polarization of macrophages but negatively regulate M2 polarization at later stages.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"684-691"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045333","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":"[Hypertension exacerbates postoperative learning and memory impairment in rats possibly due to UCP2 downregulation-mediated mitochondrial dysfunction].","authors":"Luyu Liu, Maowei Gong, Guosong Liao, Weixing Zhao, Qiang Fu","doi":"10.12122/j.issn.1673-4254.2025.04.07","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.07","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the correlation of hypertension with postoperative cognitive dysfunction and its possible mechanism.</p><p><strong>Methods: </strong>Twelve-week-old spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats were both randomized into control group and surgical group (<i>n=</i>8). In the latter group, the rats received carotid artery exposure surgery under sevoflurane anesthesia to establish models of postoperative learning and memory impairment. Postoperative cognitive function changes of the rats were evaluated using behavioral tests. The hippocampus of the rats were collected for determining ATP level and mitochondrial membrane potential (MMP) and for detecting expressions of UCP2 and astrocyte markers (GFAP and NOX4) using Western blotting and immunofluorescence staining. Serum levels of ROS, IL-6, IL-1β and TNF‑α were detected using ELISA. Nissl staining was used to examine hippocampal neuronal loss in the CA1 region.</p><p><strong>Results: </strong>The SHRs exhibited exacerbated learning and memory deficits following the surgery as shown by significantly reduced performance in novel object recognition tests and context-related and tone-related fear conditioning experiments. Compared with WKY rats, the SHRs had significantly decreased mitochondrial UCP2 expression and MMP in the hippocampus, increased hippocampal ATP level, and markedly increased serum levels of ROS and inflammatory factors, showing also increased activation of hippocampal astrocytes and microglia and reduced number of neurons positive for Nissl staining.</p><p><strong>Conclusions: </strong>Hypertension can exacerbate major postoperative learning and memory impairment in rats possibly as a result of UCP2-mediated mitochondrial dysfunction and oxidative stress damage, which further leads to astrocyte overactivation and neuronal damage.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"725-735"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971724","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":"[Cannabidiol regulates circadian rhythm to improve sleep disorders following general anesthesia in rats].","authors":"Xinshun Wu, Jingcao Li, Ying Liu, Renhong Qiu, Henglin Wang, Rui Xye, Yang Zhang, Shuo Li, Qiongyin Fan, Huajin Dong, Youzhi Zhang, Jiangbei Cao","doi":"10.12122/j.issn.1673-4254.2025.04.09","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.09","url":null,"abstract":"<p><strong>Objectives: </strong>To assess the regulatory effect of cannabidiol (CBD) on circadian rhythm sleep disorders following general anesthesia and explore its potential mechanism in a rat model of propofol-induced rhythm sleep disorder.</p><p><strong>Methods: </strong>An electrode was embedded in the skull for cortical EEG recording in 24 male SD rats, which were randomized into control, propofol, CBD treatment, and diazepam treatment groups (<i>n</i>=6). Eight days later, a single dose of propofol (10 mg/kg) was injected via the tail vein with anesthesia maintenance for 3 h in the latter 3 groups, and daily treatment with saline, CBD or diazepam was administered via gavage; the control rats received only saline injection. A wireless system was used for collecting EEG, EMG, and body temperature data within 72 h after propofol injection. After data collection, blood samples and hypothalamic tissue samples were collected for determining serum levels of oxidative stress markers and hypothalamic expressions of the key clock proteins.</p><p><strong>Results: </strong>Compared with the control rats, the rats with CBD treatment showed significantly increased sleep time at night (20:00-6:00), especially during the time period of 4:00-6:00 am. Compared with the rats in propofol group, which had prolonged SWS time and increased sleep episodes during 18:00-24:00 and sleep-wake transitions, the CBD-treated rats exhibited a significant reduction of SWS time and fewer SWS-to-active-awake transitions with increased SWS aspects and sleep-wake transitions at night (24:00-08:00). Diazepam treatment produced similar effect to CBD but with a weaker effect on sleep-wake transitions. Propofol caused significant changes in protein expressions and redox state, which were effectively reversed by CBD treatment.</p><p><strong>Conclusions: </strong>CBD can improve sleep structure and circadian rhythm in rats with propofol-induced sleep disorder possibly by regulating hypothalamic expressions of the key circadian clock proteins, suggesting a new treatment option for perioperative sleep disorders.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"744-750"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036323","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":"[High expression of DTX2 promotes proliferation, invasion and epithelial-mesenchymal transition of oxaliplatin-resistant colorectal cancer cells].","authors":"Zhennan Ma, Fuquan Liu, Xuefeng Zhao, Xiaowei Zhang","doi":"10.12122/j.issn.1673-4254.2025.04.18","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.18","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of DTX2 in regulating biological behaviors of oxaliplatin-resistant colorectal cancer cells (CRC/OXA cells).</p><p><strong>Methods: </strong>CCK8 assay was used to determine the inhibition rate of oxaliplatin-treated CRC cells. A CRC/OXA cell line was constructed, in which DTX2 expression level was detected. The cells were transfected with a DTX2-shRNA plasmid or co-transfected with DTX2-shRNA and pcDNA-Notch2, and the changes in cell proliferation, migration and invasion ability were evaluated using plate cloning assay, scratch assay and Transwell invasion assay. The expression levels of Notch2, NICD and epithelial-mesenchymal transition (EMT) proteins of the transfected cells were detected with Western blotting. In a nude mouse model bearing SW620/OXA cell xenografts, the effects of DTX2 knockdown and Notch2 overexpression in the implanted cells on tumor growth and protein expressions were tested.</p><p><strong>Results: </strong>The IC₅₀ of oxaliplatin was 6.00 μmol/L in SW620 cells and 8.00 μmol/L in LoVo cells. CRC/OXA cells showed a significantly increased expression of DTX2. DTX2 knockdown in CRC/OXA cells significantly inhibited cell proliferation, migration and invasion, and these effects were reversed by co-transfection of the cells with pcDNA-Notch2. DTX2 knockdown significantly reduced the expression levels of Notch2, NICD and vimentin proteins and increased E-cadherin expression in CRC/OXA cells, and co-transfection with pcDNA-Notch2 potently attenuated the changes in these proteins. In the tumor-bearing mice, DTX2 overexpression obviously promoted the growth of SW620/OXA cell xenograft, enhanced the protein expressions of Notch2, NICD and vimentin, and lowered the expression of E-cadherin.</p><p><strong>Conclusions: </strong>High expression of DTX2 promotes proliferation, migration, invasion and EMT of CRC/OXA cells through the Notch2 signaling pathway, suggesting the potential of DTX2 as a target to improve the efficacy of oxaliplatin.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"829-836"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025151","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":"[Early life <i>Bifidobacterium bifidum</i> BD-1 intervention alleviates hyperactivity of juvenile female rats with attention deficit hyperactivity disorder].","authors":"Yang Yang, Kai Wang, Jianxiu Liu, Zhimo Zhou, Wen Jia, Simou Wu, Jinxing Li, Fang He, Ruyue Cheng","doi":"10.12122/j.issn.1673-4254.2025.04.04","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.04","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effects of early life intervention with <i>Bifidobacterium bifidum</i> BD-1 (<i>B. bifidum</i> BD-1) on hyperactivity in a female mouse model of attention deficit hyperactivity disorder (ADHD) and explore the underlying mechanisms.</p><p><strong>Methods: </strong>Eight newborn female Wistar-Kyoto (WKY) rats and 6 spontaneous hypertensive rats (SHRs) were gavaged with saline and another 6 SHRs were gavaged with <i>B. bifidum</i> BD-1 (10⁹ CFU) daily for 3 weeks. Open field test of the rats was conducted at 7 weeks, and fecal samples were collected at weaning (3 weeks) and at 7 weeks for 16S rRNA sequencing. Immunofluorescent staining was used to detect dopamine transporter (DAT) and tyrosine hydroxylase (Th) levels in the striatum and activated microglia in the prefrontal cortex. Treg cells in the mesenteric lymph nodes, spleen and blood were analyzed using flow cytometry.</p><p><strong>Results: </strong>The SHRs traveled a significantly greater distance in open fields test than WKY rats, and this behavior was significantly attenuated by <i>B. bifidum</i> BD-1 intervention. The expression of DAT and Th in the striatum was significantly lower in the SHRs than in WKY rats, while <i>B. bifidum</i> BD-1 treatment obviously increased Th levels in the SHRs. <i>B. bifidum</i> BD-1 intervention significantly deceased the number of activated microglia and increased Treg cell counts in the spleen of SHRs. The treatment also enhanced α diversity in gut microbiota of the SHRs and resulted in a decreased <i>Firmicutes</i>/<i>Bacteroidota</i> ratio, more active <i>Muribaculaceae</i> growth, and suppression of <i>Clostridia_UCG-014</i> proliferation.</p><p><strong>Conclusions: </strong>Early life intervention with <i>B. bifidum</i> BD-1 alleviates hyperactivity in female SHRs by modulating the gut microbiota and peripheral immune response, suppressing neuroinflammation and improving dopaminergic system function. These findings provide evidence for early prevention strategies and support the development and application of psychobiotics for ADHD.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"702-710"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034083","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}