1.Ionizing Radiation-induced Lens Injury: Epidemiology, Dose-effect Relationship, and Molecular Mechanisms
Cheng-Hao HU ; Shao-Han REN ; Hai-Tao ZHANG ; Jing-Ming ZHAN
Progress in Biochemistry and Biophysics 2026;53(3):688-696
The crystalline lens of the eye is recognized as one of the most radiosensitive tissues in the human body. While the International Commission on Radiological Protection (ICRP) has classified ionizing radiation (IR)-induced cataracts as a tissue reaction (deterministic effect) and subsequently reduced the occupational equivalent dose limit for the lens, significant uncertainties remain regarding the precise dose threshold and the complex biological pathways driving lens opacification. This review provides a comprehensive synthesis of current knowledge concerning radiation-induced lens damage, integrating epidemiological exposure characteristics with dose-response modeling and mechanistic molecular insights. First, we analyze exposure characteristics through four epidemiological dimensions: dose, time, space, and population. Clinical evidence suggests that radiation cataracts—particularly posterior subcapsular opacities—exhibit a distinct latency period that is inversely correlated with dose. We highlight that risk is not confined to acute high-dose scenarios (such as in atomic bomb survivors) but is increasingly relevant in chronic low-dose occupational settings (e.g., interventional radiology) and medical diagnostics (e.g., CT scans). Crucially, individual susceptibility is modified by genetic background, age, and environmental co-factors, complicating risk assessment. Second, we critically examine the dose-effect relationship. Although the ICRP suggests a threshold of 0.5 Gy, emerging data challenge the traditional threshold model, with some studies advocating for a linear non-threshold (LNT) relationship. We further discuss the critical roles of radiation quality and dose rate. High linear energy transfer (LET) radiation demonstrates a significantly higher relative biological effectiveness (RBE) for cataractogenesis compared to low-LET radiation. Paradoxically, and unlike many other tissues, the lens may exhibit an “inverse dose-rate effect,” where fractionated or protracted exposures potentially enhance biological damage—a finding that challenges classical radiobiological paradigms. Third, drawing upon the “cataractogenic load” hypothesis and the unique physiological constraints of the lens, this review elucidates the multidimensional molecular mechanisms driving radiation-induced opacification. Key mechanisms include four aspects. (1) DNA damage and repair: IR induces DNA double-strand breaks (DSBs) that, due to the lens’ limited repair capacity (modulated by genes such as ATM, Ptch1, and Ercc2), lead to the accumulation of damage. (2) Antioxidant defense system: dysfunction of the Nrf2/HO-1 antioxidant axis results in redox imbalances, triggering NF-κB-mediated inflammation and protein aggregation. (3) Cell proliferation and senescence: IR disrupts cell cycle regulation, causing a dichotomy of effects—driving premature senescence in some cell populations (evidenced by ATM nuclear foci) while inducing aberrant proliferation via growth factor upregulation (FGF2, TGFβ) in others. (4) Cell migration and adhesion: activation of the Wnt/β‑catenin pathway and alterations in the E-cadherin complex promote the abnormal migration of epithelial cells to the posterior capsule, a hallmark of radiation-induced cataracts. In conclusion, radiation-induced cataractogenesis is a multifactorial process in which genetic susceptibility and environmental stressors converge to overwhelm the lens’ homeostatic thresholds. Future research must prioritize longitudinal cohort studies to refine dose thresholds and employ multi-omics approaches to map the crosstalk between DNA damage responses and matrix remodeling. Establishing a robust mechanistic model is essential for developing targeted radioprotective strategies and optimizing radiation protection standards for occupational and medical safety.
2.Chemical constituents from the water fraction of rhizoma of Smilax trinervula and their biological activities
Yong-hong LIANG ; Jia-cheng WANG ; Hui-lian HUANG ; Hui-ying YAO ; Yu LU ; Cheng-qi WANG ; Hai-ying ZHONG ; Ying-cai YU ; Hai-yan ZHANG
Chinese Traditional Patent Medicine 2025;47(3):807-812
AIM To study the chemical constituents from the water fraction of rhizoma of Smilax trinervula Miq.and their biological activities.METHODS Polyamide,silica gel,Sephadex LH-20,ODS and semi-preparative HPLC were used for isolation and purification,then the structures of obtained compounds were identified by physicochemical properties and spectral data.The antitumor activities were determined by MTT mothod,and the inhibitory activities on α-glucosidase were determined by PNPG method.RESULTS Eleven compounds were isolated and identified as tyrosine(1),uridine(2),2-(2',3',4'-trihydroxybutyl)-6-(2",3",4"-trihydroxybutyl)-pyrazine(3),2-(1',2',3',4'-tetrahydroxybutyl)-6-(2",3",4"-trihydroxybutyl)-pyrazine(4),2-(1',2',3',4'-tetrahydroxybutyl)-5-(2",3",4"-trihydroxybutyl)-pyrazine(5),uracil(6),2-(1',2',3',4'-tetrahydroxybutyl)-5-(1",2",3",4"-tetrahydroxybutyl)-pyrazine(7),dioscin(8),shikimic acid(9),pyrazine(10),3,4-dihydroxyphenyethyl alcohol 8-O-β-D-glycopyranoside(11).The IC50 values of compounds 8 to human breast cancer cell MCF-7 was(2.36±0.26)μg/mL,and the IC50 values of compounds 3-5 and 7 to α-glucosidase were(1.54±0.15)-(10.53±0.38)μg/mL.CONCLUSION Compounds 1-7,10 are isolated from Smilax genus for the first time,and compound 9,11 are first isolated from this plant.Compound 8 has anti-tumor activity,and compounds 3-5,7 have α-glucosidase inhibitory activities.
3.Icariin improves injury of tight junctional function by regulating balance of mTORC1 and mTORC2 in testicular Sertoli cells in naturally aging mice
Yao-ting CHENG ; Chang-cheng ZHANG ; Guo-qing FU ; Tan WANG ; Jian-min MAO ; Jian-ming SUN ; Hai-xia ZHAO
Chinese Pharmacological Bulletin 2025;41(6):1091-1098
Aim To explore the protective effect of icariin on the damage of tight junctional function of Sertoli cells in naturally aging mice and the related mechanism.Methods 15-month-old C57BL/6J male mice were randomly divided into three groups:aging model group,low-dose and high-dose icariin treatment group(5 and 20 mg·kg-1).Another 1-month-old C57BL/6J male mice were considered as adult control group(n=10).The mice in adult control group and aging model group were given the vehicle(0.5%sodi-um carboxymethyl cellulose solution)by intragastric administration,while the mice in icariin-treated groups were given different concentrations of icariin,respec-tively.After continuous administration of icariin for three months,the testes and epididymis were immedi-ately removed,weighed,and the organ index was calcu-lated.Sperm viability and sperm concentration in epi-didymis were measured.The morphological changes of testes were observed by HE staining.The ultrastructur-al changes of tight junctions of Sertoli cells were ob-served by transmission electron microscopy.The ex-pression levels of tight junction-related proteins ZO-1,Occludin,and Claudin11 of testicular Sertoli cells were detected by Western blot.The expression and localiza-tion of ZO-1,Occludin,Raptor,Rictor,p-70S6K,and p-rps6 were detected by immunofluorescence.Results Compared with the aging model group,icariin signifi-cantly increased testicular weight and its index,and ep-ididymal index,improved sperm viability and increased sperm concentration in naturally aging mice.In addi-tion,icariin improved the degeneration of testicular morphology and the damage of ultrastructure of Sertoli cell tight junction with aging.Furthermore,Western blot results showed that icariin up-regulated the expres-sion of ZO-1 and Occludin,but had no significant effect on the expression of Claudin 11.Immunofluorescence assay showed that icariin up-regulated the expression of Rictor,and down-regulated the expression of p-70S6K,p-rps6 and Raptor.Conclusions Icariin improves the tight junction damage of Sertoli cells in naturally aging mice,and its mechanism may be related to restoring the balance between mTORC1 and mTORC2.
4.Icariin improves injury of tight junctional function by regulating balance of mTORC1 and mTORC2 in testicular Sertoli cells in naturally aging mice
Yao-ting CHENG ; Chang-cheng ZHANG ; Guo-qing FU ; Tan WANG ; Jian-min MAO ; Jian-ming SUN ; Hai-xia ZHAO
Chinese Pharmacological Bulletin 2025;41(6):1091-1098
Aim To explore the protective effect of icariin on the damage of tight junctional function of Sertoli cells in naturally aging mice and the related mechanism.Methods 15-month-old C57BL/6J male mice were randomly divided into three groups:aging model group,low-dose and high-dose icariin treatment group(5 and 20 mg·kg-1).Another 1-month-old C57BL/6J male mice were considered as adult control group(n=10).The mice in adult control group and aging model group were given the vehicle(0.5%sodi-um carboxymethyl cellulose solution)by intragastric administration,while the mice in icariin-treated groups were given different concentrations of icariin,respec-tively.After continuous administration of icariin for three months,the testes and epididymis were immedi-ately removed,weighed,and the organ index was calcu-lated.Sperm viability and sperm concentration in epi-didymis were measured.The morphological changes of testes were observed by HE staining.The ultrastructur-al changes of tight junctions of Sertoli cells were ob-served by transmission electron microscopy.The ex-pression levels of tight junction-related proteins ZO-1,Occludin,and Claudin11 of testicular Sertoli cells were detected by Western blot.The expression and localiza-tion of ZO-1,Occludin,Raptor,Rictor,p-70S6K,and p-rps6 were detected by immunofluorescence.Results Compared with the aging model group,icariin signifi-cantly increased testicular weight and its index,and ep-ididymal index,improved sperm viability and increased sperm concentration in naturally aging mice.In addi-tion,icariin improved the degeneration of testicular morphology and the damage of ultrastructure of Sertoli cell tight junction with aging.Furthermore,Western blot results showed that icariin up-regulated the expres-sion of ZO-1 and Occludin,but had no significant effect on the expression of Claudin 11.Immunofluorescence assay showed that icariin up-regulated the expression of Rictor,and down-regulated the expression of p-70S6K,p-rps6 and Raptor.Conclusions Icariin improves the tight junction damage of Sertoli cells in naturally aging mice,and its mechanism may be related to restoring the balance between mTORC1 and mTORC2.
5.Identification algorithm of disease severity in patients with acute respiratory distress syndrome based on ensemble learning
Peng-cheng YANG ; Xin SHAO ; Chun-chen WANG ; Kun BAO ; Yang ZHANG ; Shi-chen DU ; Hai-feng XU
Chinese Medical Equipment Journal 2025;46(2):1-9
Objective To propose a novel identification algorithm based on ensemble learning for assessing the severity of acute respiratory distress syndrome(ARDS)to achieve continuous monitoring of the disease severity.Methods Firstly,leve-raging the open-source MIMIC-Ⅳ database,a variety of non-invasive physiological parameters of patients were extracted and subjected to preliminary preprocessing.A multivariate feature selection algorithm was employed to rank these parameters and calculate feature importance scores through weighted computation.Secondly,based on the feature importance scores,a subset search algorithm was utilized to identify the subset of features that could yield optimal performance across four machine learning algorithms:neural networks,logistic regression,AdaBoost and XGBoost.Finally,a soft voting ensemble method was designed using a generalized linear regression model to integrate the results of each single machine learning algorithm,and a multivariate ensemble learning algorithm was proposed by combining the optimal feature subsets.The algorithm proposed when used to identify the severity of ADRS was evaluated with MIMIC-Ⅳ database,and compared with the traditional algorithms.Results The sensitivity,specificity,accuracy and AUC of the algorithm were 87.15%,89.23%,88.34%and 0.923 4,respectively,all of which outperformed those of the traditional algorithms.Conclusion The ARDS severity identification algorithm based on ensemble learning is capable of achieving continuous and real-time monitoring of the severity of ARDS,thereby offering robust support for the early identification and warning of ARDS in patients.[Chinese Medical Equipment Journal,2025,46(2):1-9]
6.Bioinformatics analysis of genes associated with poor prognosis in colorectal cancer
Li-jie WANG ; Si CHEN ; Cheng CHANG ; Kai-yue GAO ; Hai-jia ZHANG
Journal of Regional Anatomy and Operative Surgery 2025;34(11):955-959
Objective To screen genes associated with poor prognosis of colorectal cancer(CRC)through bioinformatics analysis.Methods The gene expression profiles of GSE74602,GSE110223,GSE113513 and GSE141174 were obtained from Gene Expression Omnibus(GEO)database,including samples from 65 CRC tissues and 65 normal tissues.Differentially expressed genes(DEGs)between CRC tissues and normal tissues were screened out by GEO2R tool and Venn software,and the consistent genes were extracted from DEGs by Venn software.A protein-protein interaction(PPI)network was constructed by the STRING database to identify key genes,which were analyzed by Kaplan-Meier Plotter and GEPIA.Kyoto encyclopedia of genes and genomes(KEGG)pathway enrichment analysis was conducted on the 13 selected genes.Results There were 171 DEGs obtained from the four datasets,including 148 up-regulated genes and 23 down-regulated genes.Up-regulated DEGs were enriched in the redox processes,bicarbonate transport,digestion,ion trans-membrane transport,and one-carbon metabolism;and down-regulated DEGs were enriched in the positive regulation of cell proliferation.The survival curve analysis showed that 30 of the 87 genes were significantly associated with poor survival prognosis.GEPIA showed that 13 of the 30 genes were highly expressed in CRC tissues compared to normal tissues,among which MYC and FGFR3 markedly enriched in the CRC pathway.Conclusion This study identifies that MYC and FGFR3 are significantly up-regulated in CRC and closely associated with poor prognosis,suggesting that they may serve as potential prognostic markers and therapeutic targets for CRC patients.
7.Bioinformatics analysis of genes associated with poor prognosis in colorectal cancer
Li-jie WANG ; Si CHEN ; Cheng CHANG ; Kai-yue GAO ; Hai-jia ZHANG
Journal of Regional Anatomy and Operative Surgery 2025;34(11):955-959
Objective To screen genes associated with poor prognosis of colorectal cancer(CRC)through bioinformatics analysis.Methods The gene expression profiles of GSE74602,GSE110223,GSE113513 and GSE141174 were obtained from Gene Expression Omnibus(GEO)database,including samples from 65 CRC tissues and 65 normal tissues.Differentially expressed genes(DEGs)between CRC tissues and normal tissues were screened out by GEO2R tool and Venn software,and the consistent genes were extracted from DEGs by Venn software.A protein-protein interaction(PPI)network was constructed by the STRING database to identify key genes,which were analyzed by Kaplan-Meier Plotter and GEPIA.Kyoto encyclopedia of genes and genomes(KEGG)pathway enrichment analysis was conducted on the 13 selected genes.Results There were 171 DEGs obtained from the four datasets,including 148 up-regulated genes and 23 down-regulated genes.Up-regulated DEGs were enriched in the redox processes,bicarbonate transport,digestion,ion trans-membrane transport,and one-carbon metabolism;and down-regulated DEGs were enriched in the positive regulation of cell proliferation.The survival curve analysis showed that 30 of the 87 genes were significantly associated with poor survival prognosis.GEPIA showed that 13 of the 30 genes were highly expressed in CRC tissues compared to normal tissues,among which MYC and FGFR3 markedly enriched in the CRC pathway.Conclusion This study identifies that MYC and FGFR3 are significantly up-regulated in CRC and closely associated with poor prognosis,suggesting that they may serve as potential prognostic markers and therapeutic targets for CRC patients.
8.Protective effect of EGR1 on neuronal cell injury in ischemic stroke via AMPK/Nrf2 pathway
Tingyu ZHANG ; Jiaqi CHENG ; Yushi TIAN ; Ying HAI
Immunological Journal 2025;41(7):476-482
Objective To explore the mechanism by which the early growth response protein 1(EGR1)/AMP-activated protein kinase(AMPK)/nuclear factor erythroid 2-related factor 2(Nrf2)pathway improves Neuro-2a cell injury via Mendelian randomization(MR),bioinformatics and in vitro models of ischemic stroke(IS).Methods The blood proteins associated with genetic susceptibility to IS were identified based on MR analysis.Then,the GSE22255 dataset was comprehensively analyzed,including GSEA,immunoinfiltration and differential expression analysis.The transcription factors closely related to the occurrence and development of IS were identified after joint analysis with MR results,and the biological functions of key genes were further verified by in vitro experiments.Results A total of 712 proteins related to IS susceptibility were identified by MR analysis.A total of 2357 differentially expressed genes were identified from the GSE22255 dataset,and 75 intersection genes and 34 transcription factors were identified after combined analysis with MR results.In vitro experiments showed that knockdown of EGR1 expression could significantly inhibit oxygen-glucose deprivation/reperfusion(OGD/R)-induced Neuro-2a cell damage,and the mechanism might be related to the up-regulation of p-AMPK and Nrf2 protein expression.Conclusion This study integrates MR analysis,transcriptomics and in vitro experiments to reveal the potential role of 75 IS susceptibility genes and transcription factor EGR1 in the pathogenesis of IS,which provides theoretical basis for the development of therapeutic drugs for IS.
9.Mechanism of tight junctional function injury of testicular Sertoli cells induced by high-fat diet based on NF-κB/NLRP3 signaling pathway
Run-min MAO ; Hai-xia ZHAO ; Hai-li DUAN ; Zi-hui GAO ; Ya-nan QU ; Guo-qing FU ; Jian-min MAO ; Jian-ming SUN ; Chang-cheng ZHANG
Chinese Pharmacological Bulletin 2025;41(11):2134-2142
Aim To investigate the effect of high-fat diet on the tight junction function injury of Sertoli cells through the NF-κB/NLRP3 signaling pathway in mice and to explore the underlying mechanism.Methods Male C57BL/6J mice were fed with high-fat or normal diet for five months.The body and gonadal organ weight of mice were measured,and their indices were calculated.The sperm concentration,the sperm viabili-ty,the testicular histomorphology and the expression levels of tight junction proteins ZO-1,Occludin and Claudin-11 were measured.TM4 cells were treated with palmitic acid(PA)for 24 h.Cell viability was detected by CCK-8 method.Then,TM4 cells were di-vided into different groups treated with PA(0,50,100,200 and 300 μmnol·L-1),and the expression lev-els of tight junction proteins ZO-1,Occludin and Clau-din-11 were detected by Western blot.The tight junc-tion permeability of TM4 cells were detected by transepithelial electrical resistance(TEER)and FITC-dextran.The expression levels of mRNA and proteins for the NF-κB/NLRP3 pathway-related factors were de-tected by RT-qPCR and Western blot.Results The results from animal experiments showed that high-fat diet increased body weight and seminal vesicle weight of mice,and decreased testicular index,epididymal in-dex,sperm concentration and sperm motility of mice.High-fat diet also caused testicular tissue structure damage and down-regulated the expression levels of tight junction proteins ZO-1 and Occludin,without af-fecting the expression of Claudin-11.In vitro,PA sig-nificantly down-regulated the expression levels of ZO-1,Occludin and Claudin-11 in TM4 cells,increased the cell permeability,as well as up-regulated the mRNA and protein expression levels of NLRP3/NF-κB signa-ling pathway-related factors in TM4 cells.Conclusions High-fat diet can impair the function of tight junction of testicualr Sertoli cells,and the machanism may be related to the activation of the NF-κB/NLRP3 signaling pathway,resulting in Sertoli cell inflammation in mice.
10.Research on practice guideline of health conversational artificial intelligence
Cheng-yu MA ; Hai-feng WU ; Yu-hui ZHANG ; Xue-fei GU ; You-li HAN
Chinese Journal of Health Policy 2025;18(4):66-73
The development of artificial intelligence(AI)technology has provided new avenues for the public to access health information.While both domestic and international research and practical applications of health conversational AI have emerged,there remains a lack of consensus on the key issues surrounding their development.Based on a comprehensive review of domestic and international literature and multiple rounds of expert consultations,the study focuses on six issues:the definition,characteristics,application scenarios,evaluation elements,evaluation methods,as well as prospects and challenges of AI-driven health consultation systems,and develops the practice guideline for health conversational artificial intelligence.The findings aim to provide scientific reference for promoting the innovative application of AI technology in the healthcare field.

Result Analysis
Print
Save
E-mail