Objective To analyze the overall characteristics, research hotspots, and development trends of immune cell-related studies in radiotherapy for rectal cancer. Methods A systematic search was conducted by using Web of Science Core Collection to retrieve articles related to radiation therapy and immune cells in rectal cancer published from 1991 to 2024. Advanced bibliometric tools, such as VOSviewer and CiteSpace, were utilized to facilitate analysis and describe publication trends, geographic contributions, institutional affiliations, journal prominence, author collaboration, and prominent keywords. Results The annual number of relevant publications has increased steadily, showing remarkable growth over the past five years. Studies focusing on adaptive immune cells (T and B cells) account for the largest proportion of works and form the most extensive collaboration networks, reflecting the central role of T cell–mediated antitumor immunity in radiotherapy. Meanwhile, innate immune cells, including myeloid-derived suppressor cells, macrophages, monocytes, and neutrophils, are increasingly investigated for their regulatory roles in shaping the tumor immune microenvironment and influencing therapeutic responses. Among countries, China and the United States have contributed the highest number of publications and demonstrated strong academic influence. While several stable research groups have been formed, intergroup collaboration remains limited. Keyword analysis revealed that radiotherapy-induced immune modulation, tumor immune microenvironment remodeling, and treatment response have emerged as major research hotspots. Conclusion Research on immune cells in rectal cancer radiotherapy has progressed rapidly in recent years. The emphasis of this field has gradually shifted from single-treatment approaches to mechanistic studies investigating the interaction between radiotherapy and the tumor immune microenvironment. The field still demonstrates considerable potential for future research and clinical translational applications.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

Objective To elucidate the molecular mechanism of reserpine-induced depression using network toxicology,molecular docking techniques,behavioral assessments of animal models,and histopathological analyses.Methods Core targets were screened using multi-database network toxicology,followed by the construction of a protein-protein interaction network and validation of core targets through molecular docking.Sprague Dawley rats were divided randomly into control and reserpine(0.5 mg/kg)groups,and administered the corresponding treatments once daily for 4 consecutive days.Behavioral changes were assessed using the forced-swim and open-field tests.Serum neurotransmitters were quantified by enzyme-linked immunosorbent assay and neuropathological damage was observed via tissue staining.Target gene expression regulation was verified by Western blot.Results Network toxicology screening and molecular docking simulation demonstrated that reserpine exhibited significant binding affinity with the dopamine D2 receptor,cyclic-AMP response element binding protein,and serine/threonine-protein kinase 1(AKT1).Animal experiments demonstrated that reserpine-treated rats displayed depression-like behaviors,including motor inhibition(P＜0.01),with decreased serum levels of norepinephrine and 5-hydroxytryptamine(P＜0.01),respectively.Pathological observations revealed microglial proliferation in the cerebral cortex,increased apoptosis,and reduced Nissl bodies in the hippocampal CA1 region.Down-regulation of brain-derived neurotrophic factor(BDNF)in brain tissue and decreased expression of hippocampal AKT1 and phosphorylated AKT1 were also observed.Conclusions Reserpine influences monoamine transmitter metabolism and neuronal structural integrity via the inhibition of BDNF and AKT1 protein expression,resulting in depressive-like behavior and cerebral nerve damage in rats.

OBJECTIVE To evaluate the efficacy and safety of Weiyan Tongluo Granules in treating chronic atrophic gastritis(CAG)and explore its potential mechanisms.METHODS From June 2020 to December 2022,100 CAG patients with spleen defi-ciency and blood stasis syndrome were enrolled and randomly divided into a trial group(n=50)and a control group(n=50)using a random number table.The trial group received Weiyan Tongluo Granules plus a folic acid placebo,while the control group received fo-lic acid tablets plus a traditional Chinese medicine granule placebo.The treatment course for both groups was 24 weeks,with 8 and 10 dropouts in the trial and control groups,respectively.Post-treatment comparisons included OLGA/OLGIM staging reversal rates,low-grade intraepithelial neoplasia regression rate,SSDPRO-CG(Patient-Reported Outcome Scale for Chronic Gastritis in Spleen-Stomach Diseases)scores,TCM syndrome scores,and safety indicators.Serum levels of PG I,PGⅡ,PGR,and G-17 were measured via ELISA before and after treatment.Gastric mucosal p-NF-κB and CDX2 protein expression levels were analyzed by Western blot,while mRNA levels of IL-1β,IL-6,VIL1,and MUC2 were quantified via qPCR.RESULTS After treatment,the trial group showed sig-nificantly higher OLGA and OLGIM stage reversal rates than the control group(P<0.05,P<0.01),though no significant difference was observed in low-grade intraepithelial neoplasia regression.Both groups exhibited significant improvements in physiological domain scores and total SSDPRO-CG scores(P<0.01),with the trial group outperforming the control group in physiological,independence,psychological domains,and total scores(P<0.05,P<0.01).TCM syndrome scores(total and sub-items:gastric distension,pain,poor appetite,bloating)decreased significantly in both groups(P<0.01),while the trial group showed greater reductions in loose stools and dull complexion(P<0.01).After-treatment,the trial group had significantly lower TCM syndrome scores than the control group(P<0.05,P<0.01).Serum PG I,PGⅡ,PGR,G-17,gastric mucosal p-NF-κB,CDX2,and IL-1β,IL-6,VIL1,MUC2 mRNA levels improved significantly in the trial group(P<0.05,P<0.01),while the control group improved only in PGⅡ(P<0.05,P<0.01).The trial group's improvements in these biomarkers surpassed the control group's(P<0.05,P<0.01).No treatment-related adverse events occurred in either group.CONCLUSION Weiyan Tongluo Granules ameliorate gastric mucosal pathology,clinical symptoms,psychological state,and quality of life in CAG patients without significant adverse effects.Its mechanism may involve sup-pressing the NF-κB pathway to reduce IL-1β and IL-6 expression,downregulating CDX2 to inhibit VIL1 and MUC2 transcription,thereby reversing the vicious cycle of inflammation-intestinal metaplasia.

Objectives:To analyze the effects of prone position ventilation in patients receiving extracorporeal membrane oxygenation(ECMO).Methods:A systematic search was conducted in databases including CNKI,Wanfang Data,China Biomedical Literature Database,PubMed,Embase,Cochrane Library,and Web of Science,from the inception of each database to October 2024,to identify studies on prone position ventilation for ECMO patients.Two researchers independently screened the literature,extracted data,and assessed the quality of the studies.Meta-analysis was performed using RevMan 5.4 software.Results:A total of 10 studies were included in this analysis,comprising 2 randomized controlled trials and 8 cohort studies.A total of 1 513 patients were included,674 were in the prone position ventilation group and 839 were in the supine position ventilation group.Analysis results of 6 studies showed that compared with supine position ventilation,prone position ventilation could increase the successful weaning rate of ECMO(OR=1.47,95%CI:1.07-2.01,P=0.02).Analysis results of 8 studies showed that compared with supine position ventilation,prone position ventilation could prolong the duration of ECMO treatment(mean difference[MD]=4.86 days,95%CI:0.95-8.77,P=0.01).Analysis results of 6 studies showed that the length of stay in the intensive care unit in the prone position ventilation group was significantly longer than that in the supine position ventilation group(MD=5.16 days,95%CI:1.08-9.25,P=0.01).Analysis results of 5 studies showed that the total length of hospital stay in the prone position ventilation group was significantly longer than that in the supine position ventilation group(MD=7.72 days,95%CI:2.10-13.34,P<0.01).Analysis results of 6 studies showed that compared with supine position ventilation,prone position ventilation could prolong the duration of mechanical ventilation(MD=6.06 days,95%CI:0.63-11.49,P=0.03).Prone position ventilation had no obvious advantage in improving patient survival rate.Conclusions:Prone position ventilation can improve the successful weaning rate from ECMO and prolong the duration of ECMO treatment as well as the duration of mechanical ventilation,but it has no significant impact on patient survival rate.Due to the generally small sample size in the studies,further research with larger sample sizes is needed to confirm the effective impact of prone position ventilation in patients receiving ECMO treatment.

ObjectiveTo study the tumor inhibition and T helper cell （Th）1/Th2 balance regulation effect of modified Wenyang Sanjie prescription on lung cancer tumor-bearing mice and to elaborate its mechanism. MethodsA mouse model bearing a lung cancer tumor was established by subcutaneous injection of Lewis lung cancer cells into the armpit and was randomly divided into lung cancer model group， low-dose， medium-dose， and high-dose groups of modified Wenyang Sanjie prescription， and positive control group， with 12 mice per group. The low-dose， medium-dose， and high-dose groups of modified Wenyang Sanjie prescription were given modified Wenyang Sanjie prescription by dosing at 2.5， 5， 10 g·kg^-1， once a day， respectively. The positive control group was intraperitoneally injected with cisplatin （2 mg·kg^-1）， once every other day， for a total of 30 days. Serum interferon （IFN）-γ， interleukin （IL）-2， IL-4， IL-6， and IL-10 were determined by enzyme-linked immunosorbent assay （ELISA）， and spleen index， thymus index， and tumor growth inhibition rate were calculated. Tumor microvascular density was determined by immunohistochemistry， and tumor hypoxia inducible-factor （HIF）-1α， epidermal growth factor receptor （EGFR）， and vascular endothelial growth factor （VEGF） mRNA were determined by Real-time quantitative polymerase chain reaction （PCR）. The protein levels of HIF-1α， EGFR， and VEGF were determined by Western blot. ResultsCompared with lung cancer model group， IFN-γ and IL-2 were increased in the modified Wenyang Sanjie prescription groups and positive control group， while IL-4， IL-6， IL-10， spleen index， thymus index， tumor weight， and tumor microvascular density were decreased， as well as HIF-1α， EGFR， and VEGF mRNA and protein levels （P<0.05）. Compared to the low-dose group of modified Wenyang Sanjie prescription， IFN-γ and IL-2 were increased in the medium-dose and high-dose groups of modified Wenyang Sanjie prescription， while IL-4， IL-6， IL-10， spleen index， thymus index， tumor weight， and tumor microvascular density were decreased， as well as HIF-1α， EGFR， and VEGF mRNA and protein levels （P<0.05）. IFN-γ and IL-2 were increased in the high-dose group of modified Wenyang Sanjie prescription compared to the medium-dose group of modified Wenyang Sanjie prescription， and IL-4， IL-6， IL-10， spleen index， thymus index， tumor weight， and tumor microvascular density were decreased， as well as HIF-1α， EGFR， and VEGF mRNA and protein levels （P<0.05）. ConclusionModified Wenyang Sanjie prescription can significantly inhibit microangiogenesis， regulate Th1/Th2 balance， inhibit tumor growth， and significantly inhibit the progression of lung cancer in mice.

ObjectiveTo study the tumor inhibition and T helper cell （Th）1/Th2 balance regulation effect of modified Wenyang Sanjie prescription on lung cancer tumor-bearing mice and to elaborate its mechanism. MethodsA mouse model bearing a lung cancer tumor was established by subcutaneous injection of Lewis lung cancer cells into the armpit and was randomly divided into lung cancer model group， low-dose， medium-dose， and high-dose groups of modified Wenyang Sanjie prescription， and positive control group， with 12 mice per group. The low-dose， medium-dose， and high-dose groups of modified Wenyang Sanjie prescription were given modified Wenyang Sanjie prescription by dosing at 2.5， 5， 10 g·kg^-1， once a day， respectively. The positive control group was intraperitoneally injected with cisplatin （2 mg·kg^-1）， once every other day， for a total of 30 days. Serum interferon （IFN）-γ， interleukin （IL）-2， IL-4， IL-6， and IL-10 were determined by enzyme-linked immunosorbent assay （ELISA）， and spleen index， thymus index， and tumor growth inhibition rate were calculated. Tumor microvascular density was determined by immunohistochemistry， and tumor hypoxia inducible-factor （HIF）-1α， epidermal growth factor receptor （EGFR）， and vascular endothelial growth factor （VEGF） mRNA were determined by Real-time quantitative polymerase chain reaction （PCR）. The protein levels of HIF-1α， EGFR， and VEGF were determined by Western blot. ResultsCompared with lung cancer model group， IFN-γ and IL-2 were increased in the modified Wenyang Sanjie prescription groups and positive control group， while IL-4， IL-6， IL-10， spleen index， thymus index， tumor weight， and tumor microvascular density were decreased， as well as HIF-1α， EGFR， and VEGF mRNA and protein levels （P<0.05）. Compared to the low-dose group of modified Wenyang Sanjie prescription， IFN-γ and IL-2 were increased in the medium-dose and high-dose groups of modified Wenyang Sanjie prescription， while IL-4， IL-6， IL-10， spleen index， thymus index， tumor weight， and tumor microvascular density were decreased， as well as HIF-1α， EGFR， and VEGF mRNA and protein levels （P<0.05）. IFN-γ and IL-2 were increased in the high-dose group of modified Wenyang Sanjie prescription compared to the medium-dose group of modified Wenyang Sanjie prescription， and IL-4， IL-6， IL-10， spleen index， thymus index， tumor weight， and tumor microvascular density were decreased， as well as HIF-1α， EGFR， and VEGF mRNA and protein levels （P<0.05）. ConclusionModified Wenyang Sanjie prescription can significantly inhibit microangiogenesis， regulate Th1/Th2 balance， inhibit tumor growth， and significantly inhibit the progression of lung cancer in mice.

Objective To investigate the value of multimodal ultrasound combined with immune-inflammatory indicators in predicting axillary lymph node(ALN)metastasis in patients with breast cancer.Methods The clinical data of 106 breast cancer patients treated in the Ultrasound Depart-ment of Nantong Cancer Hospital from January 2023 to June 2024 were analyzed,and the patients were divided into ALN metastasis group and non-metastasis group based on postoperative pathological re-sults.Univariate and multivariate Logistic regression models were used to analyze the immune-inflam-matory indicators and ultrasound parameters in both groups.The receiver operating characteristic(ROC)curve was plotted to evaluate the predictive value of each indicator.Results Univariate anal-ysis showed significant differences between the ALN metastasis group and the non-metastasis group in terms of the neutrophil-to-lymphocyte ratio(NLR),platelet-to-lymphocyte ratio(PLR),aspect ratio,maximum tumor diameter,and Adler blood flow grade(P＜0.05).NLR,PLR,maximum tumor di-ameter,and Adler blood flow grade were independent influencing factors for predicting ALN metastasis in breast cancer(P＜0.05).The area under the curve(AUC)for predicting ALN metastasis using multimodal ultrasound combined with immune-inflammatory indicators was 0.877,with a diagnostic sensitivity of 84.7％and a specificity of 76.6％.The predictive efficacy of the combined multi-indicators was significantly higher than that of individual indicators(P＜0.05).Conclusion Multimodal ultrasound combined with immune-inflammatory indicators is associated with ALN metastasis in breast cancer patients and can provide a reference basis for clinical diagnosis,subsequent treatment,and prognosis evaluation.

OBJECTIVES: Hypoxia/reoxygenation (H/R) injury is a critical pathological process during liver transplantation. Kazinol B has known anti-inflammatory, anti-apoptotic, and metabolic regulatory properties, but its protective mechanism in H/R-induced liver injury remains unclear. This study aims to investigate the protective effects and underlying mechanisms of Kazinol B in H/R-induced hepatocyte injury. METHODS: An ischemia-reperfusion model was established in healthy adult male Sprague-Dawley rats, and an in vitro H/R model was created using cultured hepatocytes. Hepatocytes were treated with Kazinol B (0-100 μmol/L) to assess cytotoxicity and protective effects. Cell viability was evaluated using the cell counting kit-8 (CCK-8) and lactate dehydrogenase (LDH) release assays. Expression of apoptosis-related proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated death promoter (Bad), and cleaved caspase-3, was detected by Western blotting. Reactive oxygen species (ROS) levels were assessed via fluorescence probes, and inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured using enzyme-linked immunosorbent assay (ELISA). TdT-mediated nick end labeling (TUNEL) staining was performed to assess DNA damage and apoptosis. RESULTS: Kazinol B had no significant effect on hepatocyte viability at 0-50 μmol/L, but showed cytotoxicity at 100 μmol/L (P<0.05). At 0.1-20 μmol/L, Kazinol B significantly improved cell survival, reduced LDH release, decreased apoptosis, and attenuated DNA damage (all P<0.001). At 10 μmol/L, Kazinol B markedly down-regulated Bad and cleaved caspase-3 (both P<0.05), and up-regulated Bcl-2 (P<0.01). It also dose-dependently reduced ROS levels and inflammatory cytokines TNF-α and IL-1β (all P<0.01). Both in vitro and in vivo, Kazinol B inhibited activation of the c-Jun N-terminal kinase (JNK) pathway without affecting extracellular regulated protein kinase (ERK) signaling (P>0.05). TUNEL staining showed that the protective effect of Kazinol B against apoptosis was partially reversed by the JNK agonist anisomycin (P<0.01). CONCLUSIONS Kazinol B mitigates hepatocyte injury induced by H/R by inhibiting the JNK signaling pathway. Its protective effect is associated with suppression of oxidative stress and inflammation, indicating its potential as a hepatoprotective agent.
Animals ; Hepatocytes/pathology* ; Rats, Sprague-Dawley ; Male ; Rats ; Reperfusion Injury/prevention & control* ; Apoptosis/drug effects* ; Reactive Oxygen Species/metabolism* ; MAP Kinase Signaling System/drug effects* ; Cell Survival/drug effects* ; Cell Hypoxia ; Cells, Cultured