OBJECTIVE To evaluate the efficacy of Compound glutamine enteric-coated capsules in the treatment and prevention of radiotherapy- and chemotherapy-related intestinal dysfunction in patients with malignant tumors. METHODS PubMed， Embase， CNKI， and Wanfang data were searched to collect randomized controlled trial （RCT） and cohort studies comparing Compound glutamine enteric-coated capsules （experimental group） with or without other treatments versus other treatments or blank control （control group）. The search period was from the establishment of each database to November 19， 2025. After literature screening， data extraction， and quality assessment， a meta-analysis was performed using RevMan 5.4 software. RESULTS A total of 23 studies were included， involving 2 014 patients. Meta-analysis results showed that the effective rate in the experimental group was significantly higher than that in the control group， the overall incidence and moderate-to-severe incidence of radiotherapy- and chemotherapy-related intestinal dysfunction， quality of life scores， and interleukin-6 levels in the experimental group were significantly lower than those in the control group （ P ＜0.05）. However， no statistically significant differences were observed between the two groups in terms of Karnofsky Performance Status score improvement rate and tumor necrosis factor-α levels （ P ＞0.05）. The results of subgroup analysis based on different medications in the control group showed that， when used for treatment， regardless of whether patients in the control group received blank control or positive control， the efficacy in the experimental group was significantly higher than that in the control group （ P ＜0.05）. When used for prevention， compared with patients who received blank control in the control group， the overall incidence and the incidence of moderate-to-severe radiotherapy- and chemotherapy-related intestinal dysfunction in the experimental group were significantly reduced （ P ＜0.05）. No statistically significant difference was found in the overall incidence or incidences of moderate-to-severe radiotherapy- and chemotherapy-related intestinal dysfunction with positive control between the two groups （ P ＞0.05）. CONCLUSIONS Compound glutamine enteric-coated capsules can effectively treat and prevent radiotherapy- and chemotherapy-related intestinal dysfunction in patients with malignant tumors， improve patients’ quality of life， and alleviate inflammatory responses.

ObjectiveTo investigate the pharmacodynamic effects of Houshihei San （HSHS） recorded with the effects of treating wind and limb heaviness on muscle tissue injury after middle cerebral artery occlusion （MCAO） in rats through the ferroptosis pathway. MethodsThirty SD male rats were selected and randomly grouped as follows： sham， MCAO， deferoxamine mesylate， high-dose HSHS （HSHS-H， 0.54 g·kg^-1）， and low-dose HSHS （HSHS-L， 0.27 g·kg^-1）， with 6 rats in each group. A laser scattering system was used to evaluate the stability of the MCAO model， and rats were administrated with corresponding agents by gavage for 7 days. During the administration period， behavioral， imaging and other methods were used to systematically evaluate the skeletal muscle tissue injury after MCAO and the therapeutic effect in each administration group. Hematoxylin-eosin staining was employed to evaluate the cross-section of muscle cells. Subsequently， immunohistochemistry was used to detect tumor suppressor p53 and glutathione peroxidase 4 （GPX4） in the soleus tissue. Western blot was employed to determine the protein levels of p53， GPX4， myogenic differentiation 1 （MyoD1）， nuclear factor E₂-related factor 2 （Nrf2）， Myostatin， solute carrier family 7 member 11 （SLC7A11）， muscle ring-finger protein-1 （MuRF1）， and muscle atrophy F-box protein （MAFbx） to verify the therapeutic effect in each group. ResultsCompared with the MCAO group， HSHS enhanced the locomotor ability and promoted muscle regeneration， which suggested that the pharmacological effects of HSHS were related to the inhibition of muscle tissue ferroptosis to reduce the expression of muscle atrophy factors. Behavioral and imaging results suggested that compared with the MCAO group， HSHS ameliorated neurological impairments in rats on day 7 （P<0.01）， enhanced 5-min locomotor distance and postural control （P<0.01）， strengthened grasping power and promoted muscle growth （P<0.01）， stabilized skeletal muscle length and weight （P<0.01）， and increased the cross-section of muscle cells （P<0.01）. Compared with the MCAO group， HSHS promoted the increases in glutathione and superoxide dismutase content and inhibited the increase in malondialdehyde content （P<0.05，P<0.01）. Ferroptosis pathway-related assays suggested that HSHS reduced the p53-positive cells and increased the GPX4-positive cells （P<0.01）. HSHS ameliorated muscle function decline after stroke by promoting the expression of GPX4， Nrf2， SLC7A11， and MyoD1 and inhibiting the expression of p53， Myostatin， MurRF1， and MAFbx to reduce ferroptosis in the muscle （P<0.01）. ConclusionHSHS， prepared with reference to the method in the Synopsis of Golden Chamber， can simultaneously reduce the myolysis and increase the protein synthesis in the skeletal muscle tissue after ischemic stroke by regulating the ferroptosis pathway.

ObjectiveTo investigate the effect and mechanism of Polygonatum neutral polysaccharides from sibiricum （PSP-NP） on colon injury in mice with chronic obstructive pulmonary disease （COPD）. MethodsMale C57BL/6J mice were randomly divided into a control group， a COPD model group， and a PSP-NP group. The COPD model was established using smoke exposure combined with intranasal LPS administration. The PSP-NP group was simultaneously treated daily with 200 mg/kg of PSP-NP via intragastric gavage， while the other groups received an equal volume of saline. HE staining was used to observe the pathological changes in the colon. ELISA was employed to detect the levels of LPS in serum and the expressions of ZO-1， Occludin， IL-6， and TNF-α in colon tissue. UPLC-MS was used to detect the types and contents of bile acids in colonic content， and to screen for differential bile acids. Differential microbial flora were identified using 16S rRNA gene sequencing， and correlation analysis was conducted with differential bile acids. PSP-NP was combined with the differential bile acids cholic acid （CA）， and deoxycholic acid （DCA） in vitro to analyze the binding capacity of PSP-NP for CA and DCA. PSP-NP was applied to NCM460 normal colonic epithelial cells cultured in CA and DCA. Cell migration ability was assessed using the scratch assay， and the mRNA expression levels of inflammatory cytokines TNF-α， IL-6， and NF-κB were measured by RT-qPCR. ResultsPSP-NP effectively improved colonic damage in COPD model mice， enhanced mechanical barrier function， alleviated inflammatory response， and regulated abnormal changes in colonic flora and bile acid metabolism. Correlation analysis further revealed that PSP-NP regulated colonic bile acid metabolism and reduced the redundancy of secondary bile acids by increasing the relative abundance of Bacteroidota， Verrucomicrobiota， Bacteroides， and Akkermansia， while decreasing the relative abundance of Lactobacillus and Bifidobacterium. Notably， in vitro binding assays demonstrated that PSP-NP bound to differential bile acids DCA and CA， with the strongest binding capacity for DCA at 58.2%. In cellular functional studies， DCA inhibited the migration ability of colonic epithelial cells NCM460 and significantly increased the relative mRNA expression levels of inflammatory factors TNF-α， IL-6， and NF-κB. Importantly， co-treatment with PSP-NP significantly ameliorated the impact of DCA on NCM460 cells. ConclusionsPSP-NP may significantly improve colonic damage in COPD model mice. The mechanism may involve the regulation of colonic bile acid metabolism and bile acid profiles through both microbial modulation and direct binding， thereby reducing the damage caused by secondary bile acids such as DCA to colonic epithelial cells.

Objective:To evaluate long-term outcomes of endoscopic papillectomy (EP) for duodenal papillary adenomas and to identify risk factors for incomplete resection.Methods:Clinical data of 180 patients diagnosed as having duodenal papillary adenoma via postoperative pathology after EP in Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School from January 2010 to December 2022 were retrospectively analyzed. Patients were divided into two groups based on their postoperative margin status: the complete resection group (negative resection margins) and the incomplete resection group (positive/uncertain resection margins). Recurrence rates were compared between the two groups, and logistic regression analysis was performed to identify risk factors for incomplete resection.Results:Among the 180 patients included in the study, 137 underwent complete resection, and 43 had incomplete resections. Recurrence rate was significantly higher in the incomplete resection group than that in the complete resection group (30.2% VS 15.3%, χ2=4.75, P=0.029). logistic regression analysis indicated that high-grade intraepithelial neoplasia was an independent risk factor for incomplete resection ( OR=2.43, 95% CI:1.12-5.26, P=0.024). Conclusion:Patients with incomplete resection after EP have a higher recurrence rate in the long-term follow-up. High-grade intraepithelial neoplasia is an independent risk factor for incomplete resection. Close surveillance and aggressive management are warranted for patients with positive or uncertain resection margins to mitigate the recurrence risk.

Objective To describe and analyze the current status,changing trend and influencing factors of the disease burden of cervical,endometrial and ovarian cancer in China from 1990 to 2021.Methods Data on incidence,mortality,disability-adjusted life year(DALY),and other indicators for cervical,endometrial and ovarian cancer were collected from the 2021 Global Burden of Disease database.Joinpoint regression models were used to analyze time trends,and age-period-cohort(APC)models assessed their impact on incidence and mortality.Spearman correlation analysis was performed to evaluate the relationship between the sociodemographic index(SDI)and the cancer indicators.Finally,the attributable risk factors for the disease burden were analyzed.Results From 1990 to 2021,age-standardized incidence rates of cervical and endometrial cancers in China significantly increased,while ovarian cancer showed no significant change.Age-standardized mortality,DALY,and years of life lost due to premature death(YLL)decreased significantly.The disease burden was heavier in middle-aged and older groups.APC model indicated an increase in cervical cancer incidence and a decrease in mortality over time.Furthermore,the incidence risks of cervical and endometrial cancers were elevated in successive birth cohorts,whereas a lower risk was observed for ovarian cancer.Correlation analysis showed significant associations between cancer incidence and mortality with SDI.Obesity has significantly contributed to the disease burden of common gynecologic cancers in China.Conclusion Mortality rates of cervical,endometrial and ovarian cancer have declined,while the incidence of cervical and endometrial cancers has significantly increased.The trends in incidence and mortality are influenced by age,period and cohort effects.Future efforts should focus on controlling risk factors like obesity to reduce the disease burden.

Objective To investigate how puerarin affects cognitive behavior and pro-inflammatory factors in the hippocampal formation of 52％(v/v)alcohol exposure/withdrawal in mice and reveal the underlying neuroimmunological mechanism by which puerarin improves alcohol-induced cognitive dysfunction.Methods A total of 120 adult female mice were randomly divided into control,52％alcohol,puerarin+52％alcohol,and normal saline(NS)+52％alcohol groups.The cognitive function of the animals was assessed using the Morris water maze,and the expression of target proteins in the hippocampal formation was detected using Western blotting and immunohistochemi-stry.Results The cognitive ability of mice in the puerarin+52％alcohol group was significantly higher than that of mice in the 52％alcohol and NS+52％alcohol groups.At the 20th hour after alcohol withdrawal,IL-6,TNF-α,and IL-1β expressions in the hippocampal formation of the puerarin+52％alcohol group were higher than those of the 52％and NS+52％alcohol groups.However,no significant difference could be observed in the expression levels of these cytokines between the puerarin+52％alcohol and control groups.Con-clusion In a female mouse model chronically exposed to 52％alcohol,puerarin can improve cognitive dysfunction during acute alcohol withdrawal,potentially related to the involvement of puerarin in regulating pro-inflammatory factor expressions in murine hippocampus formation.

Objective:To establish a cutoff level of anti-Müllerian hormone(AMH)which could help with the di-agnosis of polycystic ovary syndrome(PCOS)in adults,and to analyze the risk factors of metabolic syndrome(MS).Methods:A retrospectively analyzed 426 PCOS patients(PCOS group)and 205 healthy controls aged 20-39 years from the Health Checkup Center of the Gynecological Endocrine Center,Hunan Maternal and Child Health Hospital from January 2021 to December 2023.AMH diagnostic validity was estimated by receiver operating characteristic(ROC)curves.Patients were subgrouped into PCOS combined metabolic syndrome group(MS-PCOS)and the uncomplicated MS group(UMS-PCOS)according to metabolic status.Multivariate Logistic regression analysis was performed to determine the risk factors for MS in PCOS patients.Results:The serum AMH level was higher in PCOS group than that in the control group(8.42±3.71 ng/ml vs.2.99±0.94 ng/ml,P＜0.001).AMH cutoff for the diagnosis of PCOS was determined as≥4.87 ng/ml on ROC analysis,and the area under the curve is 0.981 with 92.7％sensitivity and 94.6％specificity.The prevalence of MS was 18.3％(78 ca-ses)in PCOS group.Subgroup analysis showed that MS-PCOS patients had higher waist circumference,BMI,fasting glucose,dyslipidemia,hypertension(BP＞130/85 mmHg),and hormone related index androgen level,but lower AMH vs.UMS-PCOS.Multivariate Logistic regression analysis identified insulin resistance(OR 39.17,95％CI 9.33-164.48),BMI ≥24 kg/m2(OR 3.72,95％CI 1.86-7.45),and hyperandrogenism(OR 2.56,95％CI 1.34-4.89)as independent risk factors of MS.AMH was negatively associated with MS,a single-unit increase in AMH was associated with an 17％decrease in odds of MS(OR 0.83,95％CI 0.73-0.95,P=0.006).Conclusions:Serum AMH levels were significantly higher in adult PCOS patients,with an optimal diagnostic threshold of 4.87 ng/ml.Hyperandrogenism and low AMH levels may predict a higher risk of MS,in addition to metabolism-related factors.

Aim To explore the effects of apolipoprotein A Ⅰ(ApoA Ⅰ)and apolipoprotein A Ⅰ binding protein(AIBP)on THP-1-derived macrophage pyroptosis.Methods The lactate dehydrogenase(LDH)detection kit was used to evaluate cell membrane integrity,Hoechst33342/PI staining was used to observe cell membrane permeability,ELISA was used to detect the levels of inflammatory factors such as interleukin-1 β(IL-1β)and interleukin-18(IL-18),Western blot was used to detect the expression of pyroptosis-related protein nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3(NLRP3),gasdermin D(GSDMD),cleaved Caspase-1,IL-1β and IL-18.Results Oxidized low density lipoprotein(ox-LDL)upregulated the expression of NLRP3,GSDMD-N,cleaved Caspase-1,IL-1β and IL-18 in THP-1-derived macrophages in a concentration-dependent manner,and promoted the release of IL-1β,IL-18 and LDH(P＜0.05 or P＜0.01),indicating that ox-LDL induced pyroptosis in THP-1-derived macrophages in a concentration-dependent manner.Co-treatment of macrophages with ApoA Ⅰ and AIBP significantly downregulated the ex-pression of NLRP3,GSDMD-N,cleaved Caspase-1,IL-1β and IL-18,reduced the release of IL-1 β,IL-18 and LDH,and inhibited ox-LDL induced pyroptosis(P＜0.05 or P＜0.01).After ATP-binding cassette transporter A1(ABCA1)siRNA transfection,co-treatment with ApoA Ⅰ and AIBP had no significant effect on the expression of pyroptosis-related proteins and secretion of inflammatory factors(P＞0.05).Co-treatment of macrophages with ApoA Ⅰ and AIBP significantly re-duced the expression of purinergic 2X7R receptor(P2X7R)on the cell membrane,inhibited P2X7R mediated protein ki-nase R(PKR)phosphorylation and NLRP3 inflammasome assembly(P＜0.05 or P＜0.01).After P2X7R siRNA trans-fection,co-treatment with ApoA Ⅰ and AIBP had no significant effect on the expression of pyroptosis-related proteins and secretion of inflammatory factors(P＞0.05).Conclusion ApoA Ⅰ and AIBP reduce the expression of P2X7R on the cell membrane through ABCA1,inhibiting P2X7R/PKR/NLRP3 mediated macrophage pyroptosis.

Objective:Investigate key genes influencing vascular calcification through bioinformatics analysis and experimental validation.Methods:Three vascular calcification datasets (GSE159832, GSE229679 and GSE37558) were obtained from the Gene Expression Omnibus database. Subsequently, gene ontology (GO), Kyoto encyclopedia of genes and genomes (KEGG), and conventional gene set enrichment analysis (GSEA) were performed on the common differential expressed genes(DEGs). For in vitro validation, a vascular smooth muscle cell calcification model was established by stimulating mouse primary vascular smooth muscle cells with high phosphate and calcium chloride (Pi+CaCl 2). Cells were divided into a control group and a Pi+CaCl 2 group. To investigate the role of TK1, cells were transfected with TK1-targeting siRNA (siTK1) or control siRNA (siControl) prior to Pi+CaCl 2 stimulation, creating siControl+Pi+CaCl 2 and siTK1+Pi+CaCl 2 groups. The association between key DEGs and vascular calcification was assessed at the protein and mRNA levels using Western blot and quantitative real-time PCR, respectively. Changes in the phosphorylation of the downstream effector, AKT (p-AKT/AKT), were also measured. Results:A total of 2275, 449, and 381 DEGs were identified from the three vascular calcification datasets (GSE159832, GSE229679, and GSE37558), respectively. Two common DEGs-phosphoserine aminotransferase 1 and thymidine kinase 1 (TK1)-were identified across all datasets. GO enrichment analysis revealed that TK1 was significantly enriched in pathways related to ribosome biogenesis, assembly, and rRNA processing and maturation. GSEA-KEGG analysis indicated significant enrichment in the PI3K-AKT signaling pathway, pathways in cancer, neurodegenerative diseases, cytoskeleton, and smooth muscle contraction. Conventional GSEA of TK1 further confirmed significant enrichment in pathways including dynein, epithelial tight junctions, axon guidance, and vascular smooth muscle contraction pathways. At the experimental level, both protein and mRNA expression of TK1, along with the p-AKT/AKT ratio, were significantly lower in the Pi+CaCl 2 group compared to the control group (all P<0.05). Furthermore, compared to the siControl+Pi+CaCl 2 group, the siTK1+Pi+CaCl 2 group exhibited decreased expression of differentiation markers, increased expression of calcification markers, and a further reduced p-AKT/AKT ratio (all P<0.05). Conclusion:Integrated bioinformatics and cellular validation demonstrate a correlation between TK1 expression and vascular calcification, suggesting a potential protective role for TK1 in this pathological process.