Objective:To explore the the possibility and potential mechanism of Coptis chinensis in treating caries based on network pharmacology and molecular docking technology.Methods:The active ingredients of Coptis chinensis and the targets of the active in-gredients and caries were obtained through a variety of databases.The intersection targets of Coptis chinensis and caries were obtained by VENNY.Based on the target of the intersection,the protein-protein interaction(PPI)networks relationship diagram was formed on the STRING platform.The core target diagram was formed through the Cytoscape software,and the Coptis chinensis-active ingre-dient-target network diagram was constructed.The intersection targets are analyzed by GO and KEGG.The core targets of Coptis chinensis active ingredients in treating caries was analyzed by molecular docking.Results:The 11 Coptis chinensis active ingredi-ents,465 targets of Coptis chinensis active ingredients and 1 160 targets of caries were obtained from the database.After analysis,71 targets of Coptis chinensis-caries intersection and 12 core targets were obtained.The potential therapeutic effect of Coptis chinensis on caries involved relaxin,phosphatidylinositol 3-kinase-protein kinase B(PI3K-Akt),mitogen activated protein kinase(MAPK),ras-re-lated protein 1(RAP1)and other signaling pathways.Berberine,one of the main active components of Coptis chinense,had strong binding activity on epidermal growth factor receptor(EGFR),matrix metalloproteinase 9(MMP9)and other core targets.Coptis chinen-sis and its active components can play a role in the treatment of caries through EGFR,MMP9 and PI3K-AKT,MAPK and other path-ways.Conclusion:Coptis chinensis and its active components can regulate several targets and signaling pathways such as EGFR,MMP9,PI3K-AKT and MAPK.Coptis chinensis may play a role in the prevention and treatment of caries through multiple pathways.

Objective:This study investigated the dynamic expression of lipocalin-2(LCN2)and its receptor,brain-type organic cation transporter protein(BOCT),in spinal cords of hSOD1G93A transgenic mice during disease pro-gression,providing potential targets for early anti-inflammatory therapy for ALS.Methods:Utilizing hSOD1G93A trans-genic mice and their wild-type littermates(WT)as animal models,this investigation examined the expression of LCN2 and BOCT at four distinct disease stages:pre-symptomatic stage(60 d),early-symptomatic stage(95 d),symptomatic stage(108 d),and late-symptomatic stage(122 d).Spinal cords were harvested,then RT-qPCR,Western blot,and immunofluorescence double-labeling techniques were employed to assess alteration expressions of LCN2 and BOCT.Ad-ditionally,BV2 cells transfected with the pcDNA3.1-G93A-SOD1 overexpression plasmid served as an in vitro hSOD1G93A BV2 microglial model.After stimulated with LPS for 24 hours,LCN2 mRNA and protein expression in hSOD1G93A BV2 microglial cells and its culture medium were measured by RT-qPCR and ELISA respectively,while BOCT expression was measured by Western blot.Results:Compared with WT mice littermates,increased expression of LCN2 mRNA was detected in the spinal cords of hSOD1G93A transgenic mice at 108 and 122 d.No significant differences were observed in LCN2 or BOCT protein expression in the spinal cords of hSOD1G93A transgenic mice from 60 to 122 d.Double-immunofluorescence labeling revealed co-localization of LCN2 and BOCT with the microglial marker Iba-1 in the ventral horn of lumbar spinal cord of hSOD1G93A transgenic mice from 95 to 122 d.In hSOD1G93A BV2 microglial model,LPS stimulation led to a significantly increased LCN2 mRNA expression and protein secretion.Conversely,there was no significant change in BOCT protein expression after LPS stimulation.Conclusion:Our findings suggest that during ALS progression,there is an enhanced expression and release of LCN2 from activated microglia,potentially exacerbating neuroinflammation and neuronal degeneration.

Objective:This study investigated the dynamic expression of lipocalin-2(LCN2)and its receptor,brain-type organic cation transporter protein(BOCT),in spinal cords of hSOD1G93A transgenic mice during disease pro-gression,providing potential targets for early anti-inflammatory therapy for ALS.Methods:Utilizing hSOD1G93A trans-genic mice and their wild-type littermates(WT)as animal models,this investigation examined the expression of LCN2 and BOCT at four distinct disease stages:pre-symptomatic stage(60 d),early-symptomatic stage(95 d),symptomatic stage(108 d),and late-symptomatic stage(122 d).Spinal cords were harvested,then RT-qPCR,Western blot,and immunofluorescence double-labeling techniques were employed to assess alteration expressions of LCN2 and BOCT.Ad-ditionally,BV2 cells transfected with the pcDNA3.1-G93A-SOD1 overexpression plasmid served as an in vitro hSOD1G93A BV2 microglial model.After stimulated with LPS for 24 hours,LCN2 mRNA and protein expression in hSOD1G93A BV2 microglial cells and its culture medium were measured by RT-qPCR and ELISA respectively,while BOCT expression was measured by Western blot.Results:Compared with WT mice littermates,increased expression of LCN2 mRNA was detected in the spinal cords of hSOD1G93A transgenic mice at 108 and 122 d.No significant differences were observed in LCN2 or BOCT protein expression in the spinal cords of hSOD1G93A transgenic mice from 60 to 122 d.Double-immunofluorescence labeling revealed co-localization of LCN2 and BOCT with the microglial marker Iba-1 in the ventral horn of lumbar spinal cord of hSOD1G93A transgenic mice from 95 to 122 d.In hSOD1G93A BV2 microglial model,LPS stimulation led to a significantly increased LCN2 mRNA expression and protein secretion.Conversely,there was no significant change in BOCT protein expression after LPS stimulation.Conclusion:Our findings suggest that during ALS progression,there is an enhanced expression and release of LCN2 from activated microglia,potentially exacerbating neuroinflammation and neuronal degeneration.

Objective:To explore the the possibility and potential mechanism of Coptis chinensis in treating caries based on network pharmacology and molecular docking technology.Methods:The active ingredients of Coptis chinensis and the targets of the active in-gredients and caries were obtained through a variety of databases.The intersection targets of Coptis chinensis and caries were obtained by VENNY.Based on the target of the intersection,the protein-protein interaction(PPI)networks relationship diagram was formed on the STRING platform.The core target diagram was formed through the Cytoscape software,and the Coptis chinensis-active ingre-dient-target network diagram was constructed.The intersection targets are analyzed by GO and KEGG.The core targets of Coptis chinensis active ingredients in treating caries was analyzed by molecular docking.Results:The 11 Coptis chinensis active ingredi-ents,465 targets of Coptis chinensis active ingredients and 1 160 targets of caries were obtained from the database.After analysis,71 targets of Coptis chinensis-caries intersection and 12 core targets were obtained.The potential therapeutic effect of Coptis chinensis on caries involved relaxin,phosphatidylinositol 3-kinase-protein kinase B(PI3K-Akt),mitogen activated protein kinase(MAPK),ras-re-lated protein 1(RAP1)and other signaling pathways.Berberine,one of the main active components of Coptis chinense,had strong binding activity on epidermal growth factor receptor(EGFR),matrix metalloproteinase 9(MMP9)and other core targets.Coptis chinen-sis and its active components can play a role in the treatment of caries through EGFR,MMP9 and PI3K-AKT,MAPK and other path-ways.Conclusion:Coptis chinensis and its active components can regulate several targets and signaling pathways such as EGFR,MMP9,PI3K-AKT and MAPK.Coptis chinensis may play a role in the prevention and treatment of caries through multiple pathways.

Objective To explore the mechanism of ginseng in the treatment of periodontitis based on network phar-macology and molecular docking technology.Methods Potential targets of ginseng and periodontitis were obtained through various databases.The intersection targets of ginseng and periodontitis were obtained by using VENNY,the pro-tein-protein interaction network relationship diagram was formed on the STRING platform,the core target diagram was formed by Cytoscape software,and the ginseng-active ingredient-target network diagram was constructed.The selected targets were screened for gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)pathway en-richment analysis.The core targets of ginseng's active in-gredients in treating periodontitis were analyzed by mo-lecular docking technique.Results The 22 ginseng's active ingredients,591 potential targets of ginseng's ac-tive ingredients,2 249 periodontitis gene targets,and 145 ginseng-periodontitis intersection targets were analyzed.Ginseng had strong binding activity on core targets such as vas-cular endothelial growth factor A and epidermal growth factor receptor,as well as hypoxia induced-factor 1(HIF-1)sig-naling pathway and phosphatidylinositol 3-kinase-protein kinase B(PI3K-Akt)signaling pathway.Conclusion Gin-seng and its active components can regulate several signaling pathways such as HIF-1 and PI3K-Akt,thereby indicating that ginseng may play a role in treating periodontitis through multiple pathways.

In recent years,immunotherapy has become an important part of the treatment for advanced non-small cell lung cancer (NSCLC).Tumor cells can escape from the body's immune system by mediating various immune escape mechanisms,among which programmed death-1/programmed death ligand-1 (PD-1/ PD-L1) mediated immune escape plays an important role.Currently,chemotherapy,radiotherapy and molecular targeted therapy have certain limitations in the treatment of advanced NSCLC.Recent studies have found that the combined application of PD-1/PD-L1 inhibitor and other treatment methods has certain synergistic effect,thus enhances the anti-tumor effect and further prolongs the survival of patients.Immunotherapy brings not only changes in the treatment patterns of NSCLC,but also challenges in the screening of target population and the management of treatment-related adverse reactions.Summarizing the research progress on immune checkpoint inhibitors in the comprehensive treatment of advanced NSCLC can provide reference for the best treatment of NSCLC.