• Journal of Guangdong Medical University
Organizer:
Department of Education of Guangdong Province
Governing by:
Guangdong Medical University
Publishing Unit:
Department of Education of Guangdong Province
Chief Editor:
XIAO Wei
Associate Editor:
SHI Ming,XIONG Xingdong
Editorial Director:
XIONG Xingdong
ISSN:
2096-3610
   CN:
44-1731/R

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    Volume 44,2026 Issue 4

    • Abstract:Hepatocellular carcinoma (HCC) is one of the most highly prevalent and poorly prognosed malignant tumors worldwide, and surgical intervention remains the core treatment method. The conventional diagnositic and therapeutic approaches faces numerous challenges in precise assessment, individualized decision-making, and postoperative management. In recent years, artificial intelligence (AI) technology, especially the rapid development of deep learning and radiomics, has introduced systematic changes to the entire process of HCC surgical diagnosis and treatment. This article systematically reviews the latest research advancements of AI in the field of HCC surgery, clarifying its application value in enhancing diagnostic precise, informing surgical treatment decision-making and planning, formulating comprehensive treatment strategy, and improving postoperative management and prognosis prediction. Studies have shown that AI can effectively improve lesion recognition accuracy, optimize surgical strategies, reduce perioperative risks, and facilitate individualized follow-up and precise postoperative intervention. Currently, the related applications in clinical practice remain limited due to insufficient data standardization, limited external validation, and weak clinical interpretability. However, its potential to promote the development of HCC surgical diagnosis and treatment towards intelligence, precision, and individualization is enormous. In the future, further integration and standardized application of AI in liver cancer surgery should be promoted through multi-center collaboration, highquality data collaboration, and breakthroughs in interpretable AI technology, providing strong support for improving patient survival rates and quality of life.

    • Abstract:Objective To investigate the effect and mechanism of Salvianic acid A (SAA) on the proliferation and migration of human rheumatoid arthritis fibroblast-like synoviocytes (MH7A cells). Methods The effect of different concentrations of SAA on the proliferation of tumor necrosis factor-α (TNF-α)-induced MH7A cells was examined using the CCK-8 assay. The effect of SAA on the migration of TNF-α-induced MH7A cells was investigated using a scratch wound healing assay. Transcriptome sequencing analysis was employed to screen differentially expressed genes in SAAtreated TNF-α -induced MH7A cells. A protein-protein interaction (PPI) network was constructed for these genes, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to identify core genes. Molecular docking and dynamics simulations were further conducted to validate the interaction between SAA and core targets. Finally, qPCR and Western blot were used for biological validation of the core targets in the MH7A inflammatory cell model. Results TNF-α (10 μg/L) significantly induced MH7A cell proliferation (P < 0.001). Treatment with SAA at concentrations ranging from 10 to 160 µmol/L for 24, 48, and 72 hours effectively inhibited the TNF- α -induced proliferation of MH7A cells (P < 0.05). Furthermore, SAA (10 µmol/L) treatment for 24 hours significantly suppressed the TNF- α -induced migration of MH7A cells (P < 0.01). Transcriptome analysis identified 100 differentially expressed genes in SAA-treated TNF-α-induced MH7A cells. GO analysis indicated that the effects of SAA on these cells were primarily associated with focal adhesion and cadherin binding. KEGG pathway analysis suggested that the MAPK signaling pathway might be a key pathway involved in SAA's action. Molecular docking results showed a binding score of -7.290 kcal/mol between the target Superoxide dismutase 2 (SOD2) and SAA, indicating a stable and autonomous binding in silico. Molecular biological results revealed that compared to the normal group, SOD2 mRNA expression was significantly increased in TNF-α-induced MH7A cells (P < 0.0001). Compared to the model group (TNF- α alone), intervention with 10 µmol/L SAA significantly reduced SOD2 mRNA expression (P < 0.0001). Furthermore, compared with the normal group, the protein expression levels of SOD2 and CCND1 were significantly upregulated in TNF- α -induced MH7A cells (P < 0.01). Treatment with 10 µmol/L SAA significantly downregulated the protein expression of SOD2 and CCND1 (P < 0.05). Conclusion SAA can inhibit the proliferation and migration of rheumatoid arthritis fibroblast-like synoviocytes, and its mechanism may be related to the regulation of the MAPK signaling pathway and the SOD2 gene.

    • Abstract:Objective To develop a Ziyudisaponin-based lipid nanovaccine (PZONs) loaded with the model antigen ovalbumin (OVA), and to evaluate its physicochemical properties, in vitro immunostimulatory activity , in vivo ability to induce specific immune responses , and its potential as an anti-tumor vaccine platform. Methods PZONs were prepared using a double emulsion-solvent evaporation method with Ziyudisaponin, OVA, lecithin and PLGA. The morphology of the nanovaccine was characterized by transmission electron microscopy (TEM), while particle size, polydispersity index (PDI), and zeta potential were determined using a Malvern Zetasizer. The stability was evaluated in phosphate-buffered saline (PBS) and serum. Bone marrow-derived dendritic cells (BMDCs) were used to assess cellular uptake, internalization mechanisms, maturation, and antigen cross-presentation via flow cytometry and confocal microscopy. Furthermore, C57BL/6 mice were immunized subcutaneously, and serum levels of OVA-specific IgG, IgG1 and IgG2a were measured by ELISA to evaluate the systemic immune response. Results PZONs were successfully prepared with uniform morphology, exhibiting spherical or sphere-like shapes, an average particle size of 140 nm, a polydispersity index of 0.24, and a zeta potential of −11 mV. The PZONs demonstrated good stability in both PBS and serum. PZONs exhibited significant cellular uptake, which was mainly mediated by clathrin-dependent endocytosis. Compared to free OVA, PZONs significantly up-regulated the expression of co-stimulatory molecules (CD40, CD80, and MHC-II) on the surface of BMDCs and enhanced antigen cross-presentation. Furthermore, PZONs elicited significantly higher titers of OVA-specific IgG, IgG1, and IgG2a, with an increased IgG2a/IgG1 ratio indicating a Th1-based immune response.Conclusion The PZONs platform successfully induce potent, Th1 biased antigen-specific immune responses, highlighting its significant potential for anti-tumor immunotherapy.

    • Abstract:Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease the etiology of which remains incompletely understood. Its development is closely associated with the dysregulation of mucosal immune cells. Research confirms that host-microbiota interactions regulate the differentiation and effector functions of mucosal immune cells through multiple pathways, including neuro-endocrine and metabolic mechanisms. These interactions represent key targets for understanding the underlying pathogenesis and clinical management of UC. Traditional Chinese medicine (TCM) demonstrates unique therapeutic advantages due to its holistic regulation and multi-targeted interventions. TCM has demonstrated efficacy in UC by effectively improving the gut microbiome, reversing the imbalance in mucosal immune microenvironment, restoring immune cell function, and repairing mucosal damage. This review summarizes recent advances in the therapeutic efficacy and mechanisms of TCM in regulating the immune microenvironment for UC treatment. The summarized immunomodulatory mechanisms primarily involve influencing the maturation and differentiation of macrophages or dendritic cells, inhibiting the formation of neutrophil extracellular traps, and restoring immune homeostasis of the T helper cell 17 (Th17)/regulatory T cell (Treg) and Th1/Th2.

    • Abstract:Ulcerative colitis (UC) is an idiopathic inflammatory bowel disease (IBD) that affects the colon and rectum. Clinically, it is characterized by symptoms including abdominal pain, diarrhea, and bloody mucoid stools. Its pathogenesis involves the interplay of multiple factors, including genetics, environment, psychology, gut microbiota, and immune responses, and remains not fully elucidated. Acupuncture has been shown to be effective in alleviating UC symptoms, reducing disease recurrence, and improving intestinal function. Studies indicate that acupuncture can ameliorate pathological states such as spleen deficiency with excessive dampness, accumulation of damp-heat, and qi stagnation with blood stasis, thereby promoting the smooth flow of intestinal qi and harmonizing qi and blood. The underlying mechanisms may involve repairing the intestinal barrier, reducing the release of inflammatory factors including nuclear factor-kappa B and its related pathway components, and regulating gut microbiota balance.

    • Abstract:Type 2 diabetes mellitus (T2DM) is defined by insulin resistance and progressive loss of pancreatic β‑cell function. Commonly used glucose‑lowering drugs can control blood sugar, but long‑term use often leads to cumulative side effects and diminishing efficacy. In contrast, bioactive small molecules from traditional Chinese medicine differ in several ways: they are structurally diverse, act on multiple targets, exhibit relatively low toxicity, and can work through different pathways at the same time. These properties endow them with unique value in T2DM prevention and treatment. Natural compounds such as flavonoids, alkaloids, saponins, phenolic acids and terpenoids improve insulin sensitivity through multiple routes, including modulating insulin signaling, reducing oxidative stress and inflammation, and regulating gut microbiota. However, most of these natural small molecules suffer from low oral absorption and poor targeting. To address this, three structural optimization strategies have been applied: functional group modification, (de) glycosylation, and molecular skeleton remodeling. After such modifications, these compounds exhibit better solubility, membrane permeability, and metabolic stability, and their antidiabetic effects are strengthened. This article summarizes the mechanisms, structure‑activity relationships, and recent advances in structural optimization of these TCM-derived bioactive small molecules in T2DM management, providing a reference for developing and translating next-generation antidiabetic drugs based on natural products.

    • Abstract:Objective To investigate into the mechanism by which 45 ℃ hyperthermia regulates the function of chimeric antigen receptor T (CAR-T) cells and their selective effects on tumor cells through differential expression of heat shock protein 70 (HSP70). Methods Human CAR-T cells and the Raji lymphoma cell line served as in vitro models. Cells were treated with 45 ℃ hyperthermia for 15 min (experimental group) or maintained at 37 ℃ (control group), respectively. Cell viability was evaluated using the CCK-8 assay; CAR-T cell subsets (CD4 + /CD8 + ratio and CD3 + expression) were analyzed by flow cytometry; the cytotoxicity of CAR-T cells was assessed by confocal microscopy and lactate dehydrogenase (LDH) release assays; HSP70 expression levels were determined by Western blotting, and its function was verified by gene knockdown and overexpression experiments. Results Following exposure to 45 ℃ hyperthermia, the viability of CAR-T cells remained above 95%. No statistically significant differences were observed in the CD4 +/CD8 + ratio or CD3 + expression (P > 0.05). The target recognition and cytotoxic efficacy of CAR T cells against Raji cells were not significantly decreased. The relative expression level of HSP70 in CAR-T cells after hyperthermia was 4.3-fold higher than that in Raji cells (P < 0.001). Functional validation showed that knockdown of HSP70 significantly reduced the survival rate of CAR-T cells following 45 ℃ hyperthermia, whereas HSP70 overexpression enhanced their thermotolerance (P < 0.05). Conclusion Under 45 ℃ hyperthermia conditions, CAR-T cells maintained their immunophenotype and cytotoxic function, and their heat tolerance potentially attributable to differential HSP70 expression.

    • Abstract:Objective To establish intestinal epithelial-specific knockout mice of the autophagy protein gene Becn2, and to investigate the regulatory effect of intestinal epithelial-specific Becn2 deletion on intestinal epithelial cell homeostasis. Methods Becn2flox/-/Villin-Cre− mice were mated with Becn2−/−/Villin-Cre + mice. After multiple rounds of screening, control mice (Becn2fl) with the genotype Becn2flox/flox/ Villin-Cre− and knockout mice (Becn2ΔIEC) with the genotype Becn2flox/flox/Villin-Cre + were obtained. Mouse genotypes were identified by PCR, and protein-level knockout efficiency was detected by Western blot. Body weight changes were recorded from 4 to 8 weeks of age. Mouse organs were harvested to compare colon length and spleen weight between Becn2fland Becn2ΔIEC mice. Histological changes in the colon and spleen were examined by hematoxylin-eosin (HE) staining. Single-cell RNA sequencing was performed on mouse colon tissues, and bioinformatic methods were used to analyze alterations in intestinal epithelial cell subsets and key differentially expressed genes in mouse colon tissues. Results PCR and Western blot confirmed the successful establishment of control Becn2fl and knockout Becn2ΔIEC mouse models. Statistical analysis of organ data showed no significant differences in body weight, colon length, or spleen index between knockout and control mice under physiological conditions. HE staining revealed intact structure and no inflammatory lesions in the colon and spleen of both groups. Single-cell RNA sequencing analysis revealed that, compared to control mice, the proportion of goblet cells among the intestinal epithelial cell subsets decreased from 36.0% to 26.5% in Becn2 knockout mice. Furthermore, differential gene expression analysis in colonic epithelial cells revealed a slight downregulation of the Muc2 gene (log2FC =-0.51). Conclusion Under physiological conditions, intestinal epithelial-specific knockout of Becn2 does not alter the colonic tissue architecture , but reduces the proportion of goblet cells and downregulates Muc2 gene expression in colonic epithelial cells, thereby remodeling the intestinal epithelial cell composition.

    • Abstract:To compare the accuracy of domestic large language models (LLMs) in simulated clinical anesthesia emergency scenarios and to explore their application in improving clinical anesthesia emergency capabilities. Methods Questions related to clinical anesthesia emergencies were submitted to six mainstream domestic LLMs, including Doubao, ERNIE, Yuanbao, DeepSeek, Kimi and Qwen, and corresponding answers were collected. Highperformance LLMs were selected based on the accuracy of responses. A total of 40 anesthesiologists were enrolled and randomly divided into an experimental group (n = 20) and a control group (n = 20). All participants completed a questionnaire based on anesthesia emergency cases before training, and scores were calculated using unified scoring criteria. The experimental group received LLM-assisted training, while the control group adopted a traditional training mode. The training period lasted for one week, with a daily training duration of 120 ± 10 minutes. After training, another questionnaire involving different anesthesia emergency cases was administered for evaluation and scoring. The scores of the two groups were compared to assess the effectiveness of LLM-assisted training. The chi-square test was used to analyze differences in the performance of LLMs in single-choice questions; the Mann-Whitney U test was applied to compare their performance in open multiple-choice questions and overall outcomes. The independent-samples t test and Mann-Whitney U test were used to evaluate the effect of LLM-assisted training. Bonferroni correction was applied to control Type I errors. The significance level was set at α =0.05, and a corrected P < 0.05 was considered statistically significant.Results Doubao demonstrated the best performance in single-choice questions involving basic knowledge, related professional knowledge and specialized knowledge, with an average accuracy of 92.3%, and ranked first with a score of 77.5 in professional practical knowledge (open multiple-choice questions). The experimental group showed significantly greater score improvement than the control group (P < 0.05). All participants in the experimental group passed the post-training test with higher score stability, while 30% of anesthesiologists in the control group showed negative improvement in academic performance. Conclusion Mainstream domestic LLMs have attained desirable maturity and stability in clinical anesthesia emergency practice. Among them, Doubao has leading advantages in knowledge depth, applicability and accuracy. LLM-assisted training can significantly improve anesthesiologists' anesthesia emergency capabilities, with the strengths of prominent efficacy, stable training effects and low adverse risks. LLMs possess favorable application value in the field of anesthesia emergency management.

    • Abstract:Objective To investigate the clinical efficacy of the reverse sural artery neurocutaneous flap in the repair of gout-related ulcers of the foot and ankle. Methods A retrospective analysis was conducted on the clinical data of 16 patients with gout-related ulcers who underwent treatment with the reverse sural artery neurocutaneous flap in our hospital between January 1, 2020, and December 31, 2024. Patient demographics, treatment details, ulcer location, ulcer size, and the average operative time were recorded. Postoperative flap survival was assessed, and serum uric acid levels, white blood cell count, erythrocyte sedimentation rate, and high-sensitivity C-reactive protein levels were measured on admission and 7 days after surgery. Functional recovery of the lower extremity was evaluated 6 months post-surgery using the Lower Extremity Functional Scale (LEFS). Results 16 patients (15 males and 1 female), ranging in age from 38 to 71 years, with an average age of 52.2 years. The ulcers were located at the ankle in 11 cases and the dorsum of the foot in 5 cases. The area of the excised flap ranged from 6 c m × 5 cm to 13 c m × 9 cm, with an average operation time of 123.9 minutes. 15 cases (survival rate: 93.8%) had flap survival. One case had partial dermal necrosis and was repaired with skin grafting, two cases exhibited delayed wound healing due to gout stone exudation, and the wounds were gradually healed after re-debridement. One case had severe venous congestion leading to flap necrosis, and the venous compression was not relieved, and an additional flap transplantation surgery was performed. At 7 days after surgery, the blood uric acid levels, white blood cell count, hypersensitive C-reactive protein levels, and neutrophils of the patients were significantly decreased compared to those at admission (Z values were -3.517, -3.518, -3.525, -3.516, respectively, P<0.05). The average follow-up time was 8 months. The postoperative lower extremity functional scores showed significant improvement compared to pre-treatment scores (Z=-3.52, P<0.05). Conclusion The reverse sural artery neurocutaneous flap is suitable for the repair of gouty ulcers in patients with controlled blood uric acid levels, providing effective functional recovery and wound coverage.

    • Abstract:Interleukin-10 (IL-10), as a multifunctional cytokine, exhibits remarkable bidirectional regulatory properties within the tumor immune microenvironment. It can both drive tumor progression by establishing an immunosuppressive microenvironment and suppress tumor growth by activating antitumor immunity. This functional duality is orchestrated by four core variables: the cellular source, mode of production, receptor status, and tumor-specific characteristics. Its protumor effect is mainly manifested in the establishment of an immunosuppressive tumor microenvironment by down-regulating antigen presentation, as well as the activation of autocrine survival signals of tumor cells to promote tumor invasion and metastasis. In contrast, its antitumor effect exerts tumor-suppressive activity by facilitating the infiltration of CD8+ T cells into the tumor, enhancing the cytotoxic functions of effector immune cells such as CD8+ T cells and natural killer (NK) cells, and remodeling the tumor immune microenvironment. This review systematically elucidates the core mechanisms underlying the bidirectional regulation of IL-10 in tumors, summarizes the advances in preclinical studies on IL-10-based agonistic and antagonistic strategies, and analyzes the current status, key bottlenecks and optimization directions of its clinical translation, thereby providing a reference for the clinical development of IL-10-related therapeutic regimens.

    • Abstract:Chimeric antigen receptor T-cell (CAR-T) therapy, a leading strategy in tumor immunotherapy, has achieved remarkable success in the treatment of hematologic malignancies. However, single-target CAR-T therapy still faces limitations such as antigen escape, tumor heterogeneity, and immunosuppressive tumor microenvironments. In recent years, dual-targeted CAR-T therapy, by co-expressing two distinct antigen recognition domains in the same T cell, has enabled synergistic multi-antigen recognition and signal integration, demonstrating unique advantages in enhancing specificity, reducing relapse rates, and prolonging therapeutic efficacy. This review systematically summarizes the main structural types of dual-targeted CAR-T cells—including tandem, parallel, and SynNotch-regulated architectures—and discusses their differences and optimization strategies in terms of signal amplification, spatial conformation, and immune regulation. Furthermore, it highlights recent advances in the application of dual-targeted CAR-T therapy in multiple myeloma, B-cell malignancies, hepatocellular carcinoma, and glioblastoma, with a focus on its mechanisms for preventing antigen escape, improving T-cell persistence, and remodeling the tumor immune microenvironment. Finally, the review provides a perspective on future developments in structural innovation, logic-gated regulation, combination immunotherapy, and safety control. This work aims to offer a comprehensive reference and theoretical basis for the continuous optimization and clinical translation of dual-targeted CAR-T therapy.

    • Abstract:Diminished ovarian reserve (DOR) is the core pathological state leading to female fertility decline. Abnormal signaling pathways, such as mitochondrial dysfunction, oxidative stress, epigenetic regulation, autophagy, and apoptosis imbalance, are the core mechanisms of DOR. In this paper, we searched and collected relevant literature from Pubmed Central, Foreign Medical Literature Retrieval Service, and other databases over the past ten years using relevant combinations of keywords. The search keywords were ovarian reserve dysfunction, pathological mechanism, and signaling pathway. The key signaling pathways of DOR were systematically reviewed: mitochondrial dysfunction and energy metabolism imbalance, PI3K/AKT/mTOR signaling pathway, TGF-β signaling pathway, Hippo pathway, oxidative stress pathway, NF- κB inflammatory pathway, and Wnt/β -catenin pathway. We focused on the follicular activation regulatory axis, with PI3K/AKT/mTOR and Hippo pathways as the core, and the central role of a vicious cycle consisting of oxidative stress and NF-κB inflammatory pathways in DOR. Through an in-depth discussion of the roles and interaction networks of the above pathways in the occurrence and development of DOR, this review provides candidate targets for the development of targeted therapeutic drugs and also provides a theoretical basis for the establishment of new diagnostic and prognostic biomarkers.

    • Abstract:Mitochondria are essential cellular organelles involved in energy metabolism and signal regulation, playing a critical role in the normal functioning of oral tissues and the development of diseases. With advances in metabolic research and mitochondrial science, an increasing number of studies have found that mitochondrial metabolic disorders are closely related to various oral diseases, such as periodontitis, pulpitis, oral cancer, and mucosal diseases. Modulating mitochondrial metabolism may represent a novel strategy for preventing and treating these diseases. This article reviews the latest research progress of mitochondrial metabolism in oral diseases, focusing on its role in immune response, redox balance, and cell fate regulation, and discusses the possibility of using it as a therapeutic target, aiming to provide theoretical support and new directions for the prevention and precision therapy of oral diseases in the future.

    • Abstract:TFE3-rearranged renal cell carcinoma (TFE3-rRCC) is a rare subtype of kidney cancer driven by Xp11.2 translocations, characterized by molecular heterogeneity due to TFE3 gene fusions with various partner genes. This article provides a systematical review of the molecular mechanisms, diagnostic approaches, and therapeutic advances, with a particular focus on the impact of different fusion partners on clinicopathological behavior, invasive potential, and patient prognosis. We emphasize that subtyping based on the fusion partner is pivotal for advancing the management of this disease from a traditional histopathological classification towards a molecularly-driven framework. This paradigm shift is critically important for guiding individualized surgery, combination therapies of targeted agents with immunotherapy, and prognostic assessment. The implementation of a stratified diagnostic pathway that integrates morphology, immunohistochemistry, and molecular testing, holds the promise of achieving precise identification and subtyping, thereby guiding the development of future personalized treatment strategies.

    • Abstract:Cardiac surgery-associated acute kidney injury (CSA-AKI) is a frequent and serious complication after cardiac surgery, as it significantly increases the mortality rate and worsens long-term clinical outcomes. Early identification of high-risk patients and timely preventive intervention are critical for improving prognosis. This article reviews cardiac surgery-associated acute kidney injury (CSA-AKI), briefly summarizes its epidemiological characteristics.; clarifies the diagnostic criteria of the Kidney Disease: Improving Global Outcomes (KDIGO) and the newly added diagnostic dimension of subclinical acute kidney injury; elaborates on the core pathophysiological mechanisms including intraoperative renal hypoperfusion, ischemia-reperfusion injury, systemic inflammatory response, and microcirculatory disturbance; classifies risk factors throughout the perioperative period (preoperative, intraoperative and postoperative) and further distinguishes between controllable and uncontrollable factors; summarizes the clinical application status, advantages and disadvantages of novel biomarkers covering renal injury and functional types such as cystatin C, interleukin-18 and neutrophil gelatinase-associated lipocalin, as well as clinical evaluation tools capable of dynamically monitoring renal perfusion and oxygenation including renal resistive index, urinary partial pressure of oxygen and renal near-infrared spectroscopy; and also summarizes the whole-process perioperative prevention and management strategies. This review aims to provide a reference for the clinical diagnosis, treatment and subsequent research of CSA-AKI.

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