Naunyn-Schmiedeberg's archives of pharmacology最新文献

{"title":"The 11th International Conference on cGMP 2024: recent trends and developments in cGMP research -meeting report.","authors":"Miriam M Cortese-Krott, Friederike Cuello, Jan R Kraehling, Michael Russwurm","doi":"10.1007/s00210-025-04059-1","DOIUrl":"https://doi.org/10.1007/s00210-025-04059-1","url":null,"abstract":"","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Levo-corydalmine derived from Rhizoma Corydalis suppresses Ox-LDL-induced endothelial cell activation and improves vasodilatation by regulating the DDIT3-eNOS pathway.","authors":"Shaoxia Xie, Jiajie Chen, Zhuoming Li, Wenwei Luo, Shilong Zhong, Weihua Lai","doi":"10.1007/s00210-025-04110-1","DOIUrl":"https://doi.org/10.1007/s00210-025-04110-1","url":null,"abstract":"<p><p>Atherosclerosis serves as the main pathological basis of numerous cardiovascular diseases and begins with endothelial cell activation. The traditional Chinese medicine Rhizoma Corydalis has garnered significant attention for its efficacy in treating cardiovascular conditions. However, its specific molecular mechanism remains unclear. This research sought to systematically explore the effects of levo-corydalmine (l-CDL) on endothelial proinflammatory activation and the related mechanisms. Network pharmacology combined with molecular docking assays was employed to construct a compound-target-pathway network and determine the optimal binding affinities between the compounds and atherosclerosis-related targets. Additionally, experimental studies were conducted to validate the regulatory effects of l-CDL on endothelial proinflammatory activation and vascular tension. Network pharmacology and molecular docking analysis revealed that l-CDL exhibited strong binding affinities for several core atherosclerosis-related targets. The results of the CCK-8, qRT-PCR, western blot, SA-β-gal staining, and fluorescence assays revealed that l-CDL suppressed ox-LDL-induced endothelial cell activation by increasing cell viability, alleviating inflammatory and senescence marker levels, and upregulating endothelial nitric oxide synthase (eNOS) in endothelial cells. A vascular ring assay further demonstrated that l-CDL promoted endothelium-dependent vasodilation under both physiological and ox-LDL-induced pathological conditions. Mechanistically, RNA sequencing and luciferase reporter gene analyses revealed that l-CDL inhibited the transcriptional activity of DNA damage inducible transcript 3 (DDIT3) and subsequently promoted eNOS expression, and these effects can be reversed by overexpression of DDIT3. This study revealed that l-CDL enhances eNOS expression by inhibiting DDIT3 expression, thereby suppressing ox-LDL-induced endothelial cell activation and improving vasodilatation. These findings indicate that l-CDL could be a potential therapeutic agent for preventing and treating endothelial proinflammatory activation and atherosclerosis.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of anoikis in hepatocellular carcinoma therapy and the assessment of anoikis-regulatory molecules as therapeutic targets.","authors":"Hongyu Wang, Yawen Yang, Gan Zhang, Guang Yang, Ying Wang, Lu Liu, Juan Du","doi":"10.1007/s00210-025-04088-w","DOIUrl":"https://doi.org/10.1007/s00210-025-04088-w","url":null,"abstract":"<p><p>As the fourth leading cause of death from cancer and the sixth most common neoplasm in the world, hepatocellular carcinoma (HCC) is responsible for ninety percent of all primary liver cancers. There are four mechanisms that contribute to the spread of cancer: the separation of cells from the primary neoplasm, their survivability during metastasis, extravasation, and the development of secondary tumors at remote locations. In addition to its role in the development of a scaffold for cell adhesion, the extracellular matrix (ECM) also plays a role in the stimulation of signal transduction and the regulation of essential cellular mechanisms, including proliferation, migration, differentiation, and viability. The disruption of cell-ECM interactions and the ensuing separation of cells from the primary ECM trigger anoikis, a form of programmed cell death. One of the most effective factors in suppressing anoikis is ECM receptors from the integrin family. Cell migration, proliferation, and survival are primarily governed by the formation of physical connections with the cytoskeleton and the conveyance of signals between cells and the ECM via integrin receptors.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunocyte phenotypes and childhood disease susceptibility: insights from bidirectional Mendelian randomization and implications for immunomodulatory therapies.","authors":"Yanggang Hong, Yi Wang, Wanyi Shu","doi":"10.1007/s00210-025-04091-1","DOIUrl":"https://doi.org/10.1007/s00210-025-04091-1","url":null,"abstract":"<p><p>Immune cells are essential for maintaining immune homeostasis during childhood and influence both growth and disease susceptibility. However, the causal relationships between immunocyte phenotypes and childhood diseases remain unclear. This study employed a two-sample Mendelian Randomization (MR) analysis to assess causal associations between 731 immunocyte phenotypes and four major childhood diseases: childhood obesity, childhood absence epilepsy, childhood asthma, and childhood allergies. Genome-wide association study (GWAS) data were used, and stringent instrumental variable (IV) selection and multiple sensitivity analyses, including MR-Egger, weighted median, and leave-one-out tests, were applied to validate the robustness of the results. Significant associations were identified between specific T cell, monocyte, and B cell phenotypes and childhood diseases. Notably, CD8bright T cells and CD19 + B cells were positively correlated with childhood obesity, while monocyte subtypes were strongly associated with asthma pathophysiology. Reverse MR analysis indicated no significant causal effects of childhood diseases on immune phenotypes, except for negative associations between childhood asthma and TCRgd AC, and childhood allergy and CD28 + CD45RA + CD4 + cells. These findings highlight the critical role of immune dysregulation in childhood disease etiology and suggest potential targets for immunomodulatory therapies. Understanding these immune-disease interactions may inform novel pharmacological interventions, particularly in immune-mediated disorders such as asthma and obesity. Further research into immune-targeted therapies could enhance treatment strategies for pediatric conditions associated with chronic inflammation and immune dysfunction.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the therapeutic potential of tryptophan and vitamin A in modulating immune responses in celiac disease: an experimental study.","authors":"Fatemeh Asgari, Abdolrahim Nikzamir, Kaveh Baghaei, Andrea Masotti, Mohammad Rostami-Nejad","doi":"10.1007/s00210-025-04089-9","DOIUrl":"https://doi.org/10.1007/s00210-025-04089-9","url":null,"abstract":"<p><p>Dendritic cells (DCs) play a crucial role in gliadin-induced inflammation in celiac disease as they are the first immune cells to encounter gliadin. Tryptophan (Trp) and vitamin A (retinol, Ret) are known to influence the immune response of DCs to gliadin and increase their tolerogenicity. CD4 + CD25 + Foxp3 + regulatory T cells (Tregs), which are important for immune tolerance, can be generated from naive T cells in the presence of retinoic acid (RA) and TGF-β.The aim of this study was to determine the combined effect of Ret and Trp in altering the phenotypic and functional maturation of DCs by gliadin and their contribution to the differentiation of Tregs. Monocyte cells derived from the peripheral blood mononuclear cells (PBMCs) of patients with celiac disease were differentiated into DCs and stimulated with PT-gliadin. These cells were then treated with Trp + Ret. The expression of CD11c, CD14, CD83, CD86, PDL1, CD4, CD25 and FOXP3 was examined using flow cytometry. TGF-β, IL-10, IL-12, and TNF-α levels were measured by ELISA. qRT-PCR was used to quantify the mRNA levels of retinaldehyde dehydrogenase 2 (RALDH2), integrin αE (CD103), and NF-κB. Indoleamine 2,3-dioxygenase (IDO) mRNA and protein levels were assessed using qRT-PCR and Western blot assays, respectively. The maturation of DCs by PT-gliadin was defined through co-stimulatory molecule expression (CD83 and CD86) and promotion of TNF-α and IL-12 secretion. We found that after treatment with Ret + Trp, the production levels of IL-12, TNF-α, and NF-κB were significantly reduced, while the expression of IL-10, TGF-β, and the inhibitory markers PDL1, CD103, IDO, and RALDH2 by PT-gliadin-stimulated DCs was significantly increased. Furthermore, in a DC and T cell co-culture system, treatment of DCs with Ret + Trp increased TGF-β expression in DCS and promoted CD4 + CD25 + FOXP3 Treg induction. These results indicate the potential benefit of vitamin A and tryptophan as therapeutic options for individuals with celiac disease. Further research is required to fully understand the mechanisms of action of these substances in these cells.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of key immune genes of drug-induced liver injury induced by tolvaptan based on bioinformatics.","authors":"Xiyun Yang, Yuxuan Ming, Zhihui Zhou, Xinyi Zhou, Chaolong Rao","doi":"10.1007/s00210-025-04084-0","DOIUrl":"https://doi.org/10.1007/s00210-025-04084-0","url":null,"abstract":"<p><p>Drug-induced liver injury (DILI) poses critical challenges in preclinical drug development and is a primary reason for candidate drug attrition. The incidence of DILI has risen in recent years. While immune-related genes (IRGs) are crucial in immune infiltration, their expression and regulatory mechanisms in tolvaptan-induced DILI remain largely uncharacterized. RNA sequencing data related to DILI and associated clinical data were sourced from the Gene Expression Omnibus (GEO), and IRGs were obtained from the ImmPort database. Differentially expressed genes (DEGs) from DILI and IRGs were intersected to identify differentially expressed immune-related genes (DEIRGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to elucidate the biological functions of DEIRGs. In addition, a protein-protein interaction (PPI) network of DEIRGs was constructed. Immunocytes and immune regulation analyses were conducted using the CIBERSORT tool. Receiver operating characteristic (ROC) curves were constructed to assess the diagnostic accuracy of individual DEIRGs. Networks of transcription factor and microRNA co-regulation were constructed using the NetworkAnalyst database. The expression of DEIRGs in DILI samples was quantified with RT-qPCR. From GSE99878, 204 DEGs were identified, with 23 matching IRGs exhibiting significant expression differences in 17 DEIRGs. The ROC curve analysis suggested satisfactory diagnostic values for six DEIRGs. The potential gene regulatory network comprised 214 microRNAs, 257 transcription factors, and 23 DEIRGs. Finally, RT-qPCR confirmed the expression levels of nine DEIRGs, aligning with public database results. The study revealed numerous immune-related biomarkers, verifying expression in five pivotal genes (ICAM1, CXCL10, IGF1, CX3CL1, and EGFR) and highlighting four genes with notable diagnostic potential (TNFAIP3, BDNF, NR1D2, and PPARA). Additionally, it explored the roles of key biomarkers in inflammatory responses, relevant signaling pathways, and interaction networks, offering new insights into DILI diagnosis, mechanistic understanding, and treatment strategies.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of irisin in exercise-induced muscle and metabolic health: a narrative review.","authors":"Sumaya Nadhim Mohammed, Mohannad Hamid Jasim, Shahad Hisham Mahmood, Eman Naji Saleh, Alireza Hashemzadeh","doi":"10.1007/s00210-025-04083-1","DOIUrl":"https://doi.org/10.1007/s00210-025-04083-1","url":null,"abstract":"<p><p>Irisin, a myokine released during physical exercise, has emerged as a key mediator of muscle health and metabolic regulation. This review synthesizes current evidence on how aerobic exercise stimulates irisin release and its subsequent effects, including enhanced muscle mass, strength, and recovery. Additionally, irisin promotes the browning of white adipose tissue, improving fat metabolism and glucose regulation. These adaptations position irisin as a promising therapeutic target for preventing metabolic disorders and optimizing exercise protocols. By exploring human studies and mechanistic insights, this review underscores irisin's potential to address global health challenges, such as obesity and type 2 diabetes, while advancing strategies for personalized exercise interventions.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Self-nanoemulsifying drug delivery system for nebulization: fabrication and evaluation for systemic delivery of atorvastatin.","authors":"Muhammad Danish Saeed, Kifayat Ullah Shah, Muhammad Fahad, Shefaat Ullah Shah, Syed Faisal Badshah, Hassan Shah, Irfan Anjum, Gamal A Shazly, Mohammed Bourhia","doi":"10.1007/s00210-024-03494-w","DOIUrl":"10.1007/s00210-024-03494-w","url":null,"abstract":"<p><p>The study undertakes the development of an atorvastatin-loaded self-nanoemulsifying drug delivery system (SNEDDS) to improve its bioavailability. The SNEDDS were fabricated using oleic acid, Tween 80, and Span 80 by spontaneous emulsification. The SNEDDS were assessed for their particle size distribution, zeta potential, morphology, drug content, surface tension, viscosity, and drug release. The aerodynamic performance of the SNEDDS was evaluated using an Andersen cascade impactor, while the lipid-lowering potential of the SNEDDS was determined in Wistar rats using the analyzer \"Microlab 300.\" The particle size of the SNEDDS ranged from 36 to 311 nm, with a polydispersity index (PDI) of 0.25-0.40. The zeta potential of the SNEDDS fluctuated from - 29.22 to - 38.26 mV, which declined to - 4.55 mV in the case of F5. The chitosan-coated formulation (F5) exhibited a higher viscosity (22.12 mPa s) and lower surface tension (0.056 dyne/cm) than other formulations (F1-F4). The non-coated formulation exhibited a significantly higher burst drug release, followed by a sustained drug release pattern (p ≤ 0.05) as compared to the coated formulation (F5). The nebulized SNEDDS achieved a dispersed fraction of 87 to 97%, where notably higher aerosol dispersion from F4 was attributed to its smaller particle size and circularity. The inhaled fraction of nebulized SNEDDS was 74-87%. The size of the SNEDDS droplets was the primary determinant affecting the aerodynamic performance of the SNEDDS during nebulization. The chitosan-coated SNEDDS achieved a higher antihyperlipidemic effect than marketed tablets, which shows the suitability of F5 for effective systemic delivery of atorvastatin through the lung.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3829-3842"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The molecular mechanism of berberine affecting psoriasis skin inflammation by regulating keratinocyte pyroptosis via the p38 MAPK/NF-κB pathway.","authors":"Wenfang Chen, Lingzhi Ge, Chao Zhang","doi":"10.1007/s00210-024-03461-5","DOIUrl":"10.1007/s00210-024-03461-5","url":null,"abstract":"<p><p>Berberine (BBR), a Rhizoma Coptis-sourced isoquinoline alkaloid, is an effective drug for psoriasis treatment with its therapeutic mechanism remaining unclear. We delved into the mechanism of BBR affecting psoriatic skin inflammation by regulating keratinocyte pyroptosis. A psoriasis-like skin inflammation mouse model was induced by imiquimod (IMQ) and treated with BBR and a p38 activator anisomycin. Human epidermal keratinocytes (HEKs) were stimulated with five chemokines (M5) [interleukin (IL)-17A, IL-22A, oncostatin M, tumor necrosis factor-α, IL-1α] to simulate psoriasis immune microenvironment, then treated with BBR and anisomycin. Psoriasis skin lesions, skin tissue damage, cell viability and death, and gasdermin D-N (GSDMD-N) and NOD-like receptor protein 3 (NLRP3) positive cell numbers were assessed. The p38 mitogen-activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB) pathway and levels of the NLRP3/GSDMD pathway-related proteins and inflammatory factors were determined. BBR alleviated M5-induced HEK pyroptosis by inactivating NLRP3 inflammasomes. BBR inhibited the p38 MAPK/NF-κB pathway, and its effects on HEKs were partly averted by activating the p38 MAPK/NF-κB pathway. BBR repressed NLRP3 inflammasome activation and pyroptosis by inhibiting the p38 MAPK/NF-κB pathway. Collectively, BBR suppressed keratinocyte NLRP3/GSDMD pathway pyroptosis by suppressing the p38 MAPK/NF-κB pathway, thereby affecting psoriasis skin inflammation.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3843-3859"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of hydrophilic statins on adiponectin, leptin, visfatin, and vaspin levels in streptozocin-induced diabetic rats.","authors":"Hacer Kayhan Kaya, Berjan Demirtas","doi":"10.1007/s00210-024-03517-6","DOIUrl":"10.1007/s00210-024-03517-6","url":null,"abstract":"<p><p>Statins may affect glucose metabolism through adipokines. The aim of this study was to measure the effects of hydrophilic statins on the levels of several adipokines in diabetic rats. Wistar albino rats were divided into four groups: healthy control, untreated diabetic, diabetic treated with pravastatin, and diabetic treated with rosuvastatin. Diabetes was induced by intraperitoneal injection of STZ. Thereafter, 20 mg/kg/day doses of either pravastatin or rosuvastatin were administered to the treated diabetic rats for 8 weeks. At the end of the experiment, the body weights, fasting blood glucose levels, serum insulin levels, and insulin resistance, as well as the serum adiponectin, leptin, visfatin, and vaspin levels, were measured. Fasting blood glucose and insulin resistance levels were significantly higher, whereas insulin levels and body weight were significantly lower in the untreated diabetic group than in the control group. Diabetes caused significant decreases in adiponectin, leptin, and vaspin levels but a significant increase in visfatin levels. Pravastatin treatment significantly increased body weight and decreased fasting blood glucose levels, whereas rosuvastatin decreased body weight but did not affect fasting blood glucose levels. Pravastatin caused significant increases in both adiponectin and vaspin levels. However, rosuvastatin did not affect the adiponectin level but caused a significant decrease in the vaspin levels. Both pravastatin and rosuvastatin treatments decreased the leptin and visfatin levels. In conclusion, pravastatin is more effective at improving fasting blood glucose levels and body weight in diabetic rats, probably by increasing adiponectin and vaspin levels.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3977-3984"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}