Objective To explore the molecular mechanism by which Schisandra chinensis lignans (SCL) improve neuronal apoptosis and mitochondrial damage in the sleep deprivation (SD) model rats. Methods Forty-eight rats were divided into 6 groups: Control group, SD group, modafinil ( MOD) group ( positive control), and SCL treatment groups at different concentrations. The Morris water maze and Y-maze tests were used to assess the escape latency and behavioral accuracy of rats in each group, respectively. HE staining was used to detect hippocampal tissue pathological damage in rats, and TUNEL staining was used to detect cell apoptosis. JC-1 staining and ELISA were used to detect the levels of mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) in rats’brain tissues and cells. An in vitro neuronal damage model was established using the ROS inducer 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ) to stimulate HT-22 cells. CCK-8 was used to measure cell viability. Western blotting was used to detect the expression levels of TLR4, MyD88, and p-NF-κB P65 in cells. Results Compared with those in the Control group, the escape latency of SD rats increased, and behavioral accuracy decreased. In contrast, rats treated with Mod or SCL showed reduced escape latency and increased behavioral accuracy (all P<0.05). Additionally, compared with rats in the Control group, rats in the SD group exhibited significant hippocampal tissue pathological damage, increased cell apoptosis, decreased MMP levels, and increased ROS levels. Mod or SCL intervention improved hippocampal tissue damage and cell apoptosis and reduced neuronal mitochondrial damage in SD rats (all P< 0. 05). Cellular experimental results showed that HT-22 cells in the DMNQ group had reduced viability, increased apoptosis, and increased mitochondrial damage and ROS levels when compared with those in the Control group. Mod or SCL treatment significantly improved the DMNQ-induced HT-22 cell damage. Moreover, compared with those in the Control group, the protein expression levels of TLR4, MyD88, and pNF-κB P65 in the DMNQ group cells were elevated, and Mod or SCL intervention significantly suppressed the levels of TLR4, MyD88, and p-NF-κB P65 in DMNQ-treated HT-22 cells. Conclusion SCL improves neuronal apoptosis and mitochondrial damage in SD rats by inhibiting the activation of the TLR4-MyD88-NF-κB pathway.

Objective To explore the clinical significance of EGFR expression and amplification in tongue squamous cell carcinoma. Methods Detection of EGFR using immunohistochemistry and FISH was conducted in 34 cases of tongue squamous cell carcinoma and their adjacent tissues, along with one case of pseudoepitheliomatous hyperplasia of the tongue in tissue chips. Results The expression and amplification rates of EGFR in tongue squamous cell carcinoma were higher than those in adjacent normal tissues. Specifically, the expression rate of EGFR in cancer tissues was 63. 6 % (21 out of 33 samples), while in normal tissues, it was 0 % (0 out of 33 samples). Regarding amplification, the rate in cancer tissues was 5. 9 % (2 out of 33 samples), whereas it remained at 0 % (0 out of 33 samples) in normal tissues. EGFR expression was not associated with age, gender, tissue grading, or clinical stage, but it was associated with lymph node metastasis. Conclusion: Detection of EGFR is important for differentiating tongue squamous cell
carcinoma in clinical pathology. The overexpression of EGFR protein is partially due to an increase in copy number, and an elevated level of EGFR indicates a poor clinical prognosis.

Objective To investigate the effect and mechanism of overexpression of microRNA-193b-5p ( miR-193b-5p) on cisplatin ( DDP) -resistant cell line SiHa / DDP in human cervicalcancer. Methods Human cervical cancer cell line ( SiHa) and its cisplatin-resistant cell line( SiHa / DDP) were cultured. The survival rates of the two cell lines treated with DDP (5, 10, 15, 20, 25, 30 μmol / L) were detected by MTT assay, and the half inhibitory concentration ( IC50 ) value was determined. Cells were divided into 4 groups: SiHa group, SiHa / DDP group, mimics NC group ( SiHa / DDP cells transfected with mimics NC), miR-193b-5p mimics group ( SiHa / DDP cells transfected with miR-193b-5p mimics). The expression level of miR-193b-5p was detected by RT-qPCR. Cells were then treated with DDP, and the cell survival rate and apoptosis rate were detected by the MTT method and flow cytometry. The expression of microtubule-associated protein 1 light chain 3 B (LC3B) was detected by cell immunofluorescence staining, and the protein expression levels of LC3Ⅱ / LC3Ⅰ , Beclin-1, and P62 were detected by Western blotting. Results Thesurvival rate of SiHa / DDP cells was higher than that of the SiHa cells when treated with DDP at thesame concentration (P< 0. 05), and the IC50 value of cells was significantly increased (P< 0. 05).The relative expression level of miR-193b-5p in the SiHa / DDP cells was significantly downregulated(P< 0. 05). The relative expression level of miR-193b-5p in the miR-193b-5p mimics group was higher than that in the control group and mimics NC group (P< 0. 05). Compared with those in theSiHa / DDP group and the mimics NC group, the survival rate of SiHa / DDP cells in the miR-193b-5p mimics group was significantly decreased, the apoptosis rate was significantly increased ( P <0. 05), the fluorescence intensity of LC3B in cells was significantly weakened, the LC3Ⅱ / LC3Ⅰratio and the relative expression level of Beclin-1 protein were significantly downregulated ( P <0. 05), and the relative expression level of P62 protein was significantly upregulated (P < 0. 05).Conclusion The expression level of miR-193b-5p was decreased in the cisplatin-resistant cell lineSiHa / DDP of human cervical cancer. Its overexpression could reverse the resistance of SiHa / DDPcells to DDP, which may be related to its inhibition of cell autophagy.

Objective To analyze the expression level of recombinant ependymin-related protein 1 (EPDR1) in gastric cancer ( GC) and its relationship with the prognosis of GC patients,and to further explore the effect of EPDR1 on the invasive and migrative abilities of GC cells and itspotential mechanism. Methods The expression levels of EPDR1 in gastric cancer tissues and adjacent non-cancerous tissues from the GSE62254 dataset of the GEO database and TCGA-GTEx were analyzed, and their associations with clinicopathological characteristics and prognosis of corresponding patients were investigated. Gene set enrichment analysis (GSEA) was used to explore the signaling pathways that EPDR1 might regulate in GC. The effects of EPDR1 on the migration and invasion of GC cells and its potential mechanism were investigated by RT-qPCR, Western blotting, immunofluorescence, and Transwell assay. Results Bioinformatics analysis showed that EPDR1 was significantly overexpressed in both the primary and peritoneal metastases of GC, and its high expression was closely related to poor disease-free survival and overall survival of GC patients. GSEA analysis indicated that EPDR1 may participate in the occurrence and development of GC by activating theWnt / β-catenin signaling pathway. In vitro cell experiments showed that overexpression of EPDR1 enhanced the migrative and invasive abilities of GC cells, and activated the Wnt / β-catenin pathway topromote the up-regulation of CTNNB1 protein and endonuclear translocation. Conclusion EPDR1is highly expressed in GC, which is closely related to the invasion, migration, and poor prognosis of GC, and can be used as a prognostic biomarker and potential therapeutic target for GC.

Objective To elucidate the molecular mechanism of lncRNA ANRIL in regulating the invasion and stem cell-like characteristics of ovarian cancer, and to analyze its dual role in mediating chemotherapy resistance and tumor recurrence. Methods ANRIL stable knockdown SKOV-3cell model was established (Control group, shRNA-NC group, ANRIL-shRNA1 group). The ability of cell invasion and metastasis was evaluated by Transwell assay, wound-healing assay, and the expression of VEGF and Fibronectin. The characteristics of stem cells were analyzed by tumor sphere formation assay combined with stem-cell marker CD44 / SOX2 / OCT4 detection. The targeting interaction between ANRIL-shRNA1 and miR-324-5p was verified by dual luciferase reporter assay. A functional recovery experiment ( ANRIL-shRNA1 + miR-324-5p inhibitor co-transfection group) was designed to clarify the mediating effect of miR-324-5p on the regulation of VEGF and CD44 by ANRIL-shRNA1. Results  ANRIL knockdown decreased the invasion and migration ability of SKOV-3cells, and the expression levels of VEGF and Fibronectin were significantly down-regulated. At the same time, the number of spheres was decreased, and the expression levels of CD44, SOX2, and OCT4 were decreased significantly compared with those in the control group. Dual luciferase assay confirmed that ANRIL directly binded to miR-324-5p. The inhibition of miR-324-5p could reverse the inhibitory effect of ANRIL knockdown on VEGF and CD44. Conclusion LncRNA ANRIL can promote cell invasion and help maintain the characteristics of tumor stem cells by targeting miR-324-5p.

Objective To explore the application of serum interferon-gamma-induced protein10 (IP-10), interleukin-2 (IL-2), monocyte chemoattractant protein-1 ( MCP-1), and interferon-gamma (INF-γ) in the diagnosis of active tuberculosis (ATB). Methods The clinical data of110 ATB patients who visited Hongya County Traditional Chinese Medicine Hospital from November2023 to November 2024 were retrospectively analyzed as the observation group. Another 90 patientswith other lung diseases and 60 healthy individuals undergoing physical examinations during thesame period were selected as the lung disease group and the control group, respectively. The levelsof serum IP-10, IL-2, MCP-1 and INF-γ in the three groups were compared. The relationship between IP-10, IL-2, MCP-1, INF-γ and ATB was analyzed, and the receiver operating characteristic (ROC) curve was drawn to explore the diagnostic value of IP-10, IL-2, MCP-1, and INF-γfor ATB. Results The levels of IP-10, IL-2, MCP-1, and INF-γ in the observation group werehigher than those in the lung disease group and the control group (P< 0. 05); the levels of IP-10,IL-2, MCP-1, and INF-γ in the lung disease group were higher than those in the control group(P< 0. 05). ROC curve analysis showed that the combined diagnosis of ATB with IP-10, IL-2, MCP-1, and INF-γ (AUC: 0. 813, 95 % CI: 0. 784-0. 842) was superior to the single indicators of IP-10 ( AUC: 0. 663, 95 % CI: 0. 645-0. 681), IL-2 ( AUC: 0. 627, 95 % CI: 0. 611- 0. 643), MCP-1 (AUC: 0. 721, 95 % CI: 0. 685-0. 757), and INF-γ ( AUC: 0. 734, 95 % CI: 0. 692-0. 776) ( P < 0. 05). Logistic analysis revealed that elevated IP-10 ( OR: 3. 435, 95 % CI: 1. 874-4. 996 ), elevated IL-2 ( OR: 1. 314, 95 % CI: 1. 264-6. 178 ), elevated MCP-1 (OR: 3. 691, 95 % CI: 2. 521-5. 561), and elevated INF-γ ( OR: 3. 710, 95 % CI:1. 584-5. 836) were independent risk factors for the occurrence of ATB (P< 0. 05). Conclusion IP-10, IL-2, MCP-1, and INF-γ are highly expressed in ATB, and elevated levels of IP-10, IL-2, MCP-1, and INF-γ are risk factors for the occurrence of ATB. The combined use of IP-10, IL-2, MCP-1, and INF-γ in the diagnosis of ATB can improve the accuracy of the results.

Objective To explore the effect of microRNA-377-3p ( miR-377-3p) on the proliferation and mitochondrial function of epithelial ovarian cancer (EOC) SKOV3 cells by targetingE-box binding zinc finger protein 2 (ZEB2). Methods SKOV3 cells were cultured in vitro, cellswith miR-377-3p and ZEB2 overexpression were constructed, and the proliferation, apoptosis, mitochondrial membrane potential, and oxidative stress in cells were detected. Results The expression level of ZEB2 was inhibited by miR-377-3p. Compared with those in the control group, the number of colony formation was decrease, the expression levels of Ki67, PCNA, Survivin, and the level of SOD were decreased in the miR-377-3p group, while the apoptosis rate, the proportion of JC-1 green fluorescence, the level of MDA, and the ratios of Bax / Bcl-2, cleaved caspase-3 /caspase-3 and cleaved caspase-9 / caspase-9 were increased (P < 0. 05). In addition, the number ofcolony formation, the expression levels of Ki67, PCNA, Survivin, and the level of SOD were increased in the ZEB2 group, while the apoptosis rate, proportion of JC-1 green fluorescence, the level of MDA, and the ratios of Bax / Bcl-2, cleaved caspase3 / caspase3 and cleaved caspase9 /caspase9 were decreased ( P < 0. 05 ). The overexpression of ZEB2 in the miR-377-3p + ZEB2 groups could partially reverse the effect of miR-377-3p (P < 0. 05). Conclusion miR-377-3p caninhibit the ZEB2 expression, reduce the membrane potential, enhance the oxidative stress, inhibit the proliferation, and promote the apoptosis of ovarian cancer SKOV3 cells.

Objective To explore the effect of adiponectin on the proliferation, invasion, andphosphatidylinositol 3-kinase / protein kinase B / nuclear factor kappa B (PI3K / AKT / NF-κB) pathway in endometrial cancer cells. Methods Endometrial cancer cell lines AN3CA and HEC-1-Awere transfected with pcDNA, pcDNA-adiponectin. The efficiency of adiponectin overexpression were detected by RT-PCR and Western blotting. Cell proliferation, cell apoptosis, and cell invasion were detected by CCK8, flow cytometry, and Transwell assay, respectively. The expression levels of caspase-9, caspase-3, vascular endothelial growth factor ( VEGF), E-cadherin, N-cadherin, fibronectin ( FN ), p-PI3K / PI3K, p-AKT / AKT, p-P65 / P65 were detected by Western blotting. Results Compared with those in the Control group, the adiponectin expression levels of endometrial cancer cells AN3CA and HEC-1-A in the adiponectin group were significantly increased(P < 0. 05), the cell proliferation ratio was significantly reduced (P < 0. 05), and the rate of apoptosis was significant increase (P < 0. 05), cell invasion number was significantly reduced (P <0. 05), the expression levels of caspase-9 and caspase-3 were significantly increased (P < 0. 05),VEGF levels were significantly decreased (P< 0. 05), E-cadherin level was increased, N-cadherinand FN levels were decreased (P< 0. 05), phosphorylated PI3K / AKT / P65 levels were significantly decreased (P< 0. 05). Conclusion Adiponectin inhibits the proliferation and invasion of endometrial cancer AN3CA and HEC-1-A cells and the activation of PI3K / AKT / NF-κB pathway.

Objective To investigate the effect of signal transducer and activator of transcription 3 (STAT3) on the proliferation and autophagy of colorectal cancer stem cells. Methods The colorectal cancer stem cells were sorted out from colorectal cancer cells, and were categorized into 4groups: CCSC, STAT3, STAT3 ihibitor, and STAT3 inhibitor + Wnt / β-catenin-inhibitor. The proliferation rate, apoptosis rate, and the expression levels of proteins related to cell proliferation, apoptosis, and autophagy, as well as Wnt / β-catenin signaling pathway proteins, were measured ineach group. Results The expression levels of STAT3 in cancer tissues and CD133 + CD44 + cellswere significantly higher than those in the adjacent tissues and CD133 - CD44 - cells ( P < 0. 05). Compared to the CCSC group, the STAT3 group showed increased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as higher proliferation rates, while the apoptosis rate and the expression levels of Caspase-3, Bax, and Beclin1 were reduced. Compared to both the CCSC and STAT3 groups, the STAT3 ihibitor group and the STAT3 inhibitor + Wnt / β- catenin-inhibitor group showed decreased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as lower proliferation rates, while the apoptosis rate and the expression of Caspase-3, Bax, and Beclin1 were increased (P < 0. 05). Compared to the STAT3 ihibitorgroup, the STAT3 inhibitor + Wnt / β-catenin-inhibitor group showed decreased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as lower proliferation rates, while the apoptosis rate and the expression levels of Caspase-3, Bax, and Beclin1 were increased(P< 0. 05). Conclusion Downregulation of STAT3 inhibits the proliferation, and enhances the apoptosis and autophagy of colorectal cancer stem cells. The mechanism may be related to the inhibition of the Wnt / β-catenin signaling pathway.

Fruquintinib is a novel and highly selective inhibitor of vascular endothelial growthfactor receptor (VEGFR), which plays an important role in the comprehensive treatment of colorectal cancer (CRC). Numerous studies have shown that fruquintinib can effectively block tumor angiogenesis and has demonstrated significant efficacy and good tolerance in the treatment of metastatic CRC. This review aims to summarize and discuss the pharmacological mechanism, pharmacokinetic characteristics, adverse event of fruquintinib, as well as the results of a series of clinical trials in CRC. Additionally, this review explores the potential of combining VEGFR inhibitors with other therapies, providing new directions for further optimizing its use in personalized treatment.

The long interspersed nuclear element-1 ( LINE-1) is the only retrotransposon inthe human genome capable of autonomous activity, and it plays an essential role in regulating many physiological processes. Its activity is closely connected to cellular aging and the overall aging of theorganism. Normally, LINE-1 remains tightly suppressed through epigenetic mechanisms such asDNA methylation. However, during aging or cellular stress, this control can become disrupted,leading to abnormal activation of LINE-1. When activated inappropriately, LINE-1 can cause harmthrough several pathways, including creating DNA double-strand breaks, inserting itself into new locations in the genome ( insertional mutagenesis), and triggering the cGAS-STING immune response pathway. These effects contribute to genomic instability and promote the formation of the senescence-associated secretory phenotype ( SASP). Collectively, these processes worsen telomere dysfunction and increase the risk of age-related diseases like cancer, neurodegenerative conditions,and heart disease. This review emphasizes how dysregulated LINE-1 activity considerably contributesto aging and related diseases. It focuses on its main mechanisms, particularly how it accelerates disease progression by destabilizing the genome and altering epigenetic regulation. What ’ s more,LINE-1 shows promise as a biomarker for age-associated conditions and as a potential target for therapeutic intervention.

While artificial intelligence ( AI) textbooks offer the advantage of enabling largescale personalized teaching, they face the new challenge of difficulty in visualizing massive learning data. This study systematically analyzed the learning behaviors of 436 students using the AI textbookMedical Biochemistry, addressing three critical challenges in data visualization: ① visualizing interclass variations across parallel large classes; ② analyzing the fine-grained subgroup learning profiles within a parallel large class; ③ profiling the in-depth thinking reflected in AI interactions within a parallel large class. In this research, seven key parameters were used to demonstrate the differences in learning characteristics between parallel large classes. Within one parallel large class, students were subdivided into 9 subgroups based on behavioral heterogeneity, with personalized differences analyzed across subgroups. Using a self-developed scaffold questioning framework for AI interactions, cluster analysis was conducted on all interaction questions between students and AI in one parallel large class, enabling visual evaluation of students’in-depth thinking effects. Future research should develop an automatic display for AI textbook data visualization based on these strategies to support data-driven decision-making in large-scale personalized teaching.