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当代医学科学(英文)
当代医学科学(英文)

龚菲力；冯敢生

双月刊

2096-5230

jtmu@tjmu.edu.cn

027-83692514

430030

武汉市航空路13号同济医学院学报

当代医学科学(英文)/Journal Current Medical ScienceSCI
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    Naringin and Naringenin:Potential Multi-Target Agents for Alzheimer's Disease

    Jing LUJie CHENShu-yue LIGuang-jie PAN...
    867-882页
    查看更多>>摘要：Alzheimer's disease(AD)is one of the most common forms of neurodegenerative dementia.The etiology of AD is multifactorial,and its complex pathophysiology involves tau and amyloid-β deposition,increased oxidative stress,neuroinflammation,metabolic disorders,and massive neuronal loss.Due to its complex pathology,no effective cure for AD has been found to date.Therefore,there is an unmet clinical need for the development of new drugs against AD.Natural products are known to be good sources of compounds with pharmacological activity and have potential for the development of new therapeutic agents.Naringin,a naturally occurring flavanone glycoside,is predominantly found in citrus fruits and Chinese medicinal herbs.Mounting evidence shows that naringin and its aglycone,naringenin,have direct neuroprotective effects on AD,such as anti-amyloidogenic,antioxidant,anti-acetylcholinesterase,and anti-neuroinflammatory effects,as well as metal chelation.Furthermore,they are known to improve disordered glucose/lipid metabolism,which is a high risk factor for AD.In this review,we summarize the latest data on the impact of naringin and naringenin on the molecular mechanisms involved in AD pathophysiology.Additionally,we provide an overview of the current clinical applications of naringin and naringenin.The novel delivery systems for naringin and naringenin,which can address their widespread pharmacokinetic limitations,are also discussed.The literature indicates that naringin and naringenin could be multilevel,multitargeted,and multifaceted for preventing and treating AD.
      原文链接:
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    Research Advancements in the Interplay between T3 and Macrophages

    Liu YANGMeng-fei FUHan-yu WANGHui SUN...
    883-889页
    查看更多>>摘要：3,3',5-Triiodo-L-thyronine(T3)is a key endocrine hormone in the human body that plays crucial roles in growth,development,metabolism,and immune function.Macrophages,the key regulatory cells within the immune system,exhibit marked"heterogeneity"and"plasticity",with their phenotype and function subject to modulation by local environmental signals.The interplay between the endocrine and immune systems is well documented.Numerous studies have shown that T3 significantly target macrophages,highlighting them as key cellular components in this interaction.Through the regulation of macrophage function and phenotype,T3 influences immune function and tissue repair in the body.This review comprehensively summarizes the regulatory actions and mechanisms of T3 on macrophages,offering valuable insights into further research of the immunoregulatory effects of T3.
      原文链接:
    • NETL
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    Michael Acceptor Pyrrolidone Derivatives and Their Activity against Diffuse Large B-cell Lymphoma

    Bi-qiong ZHANGFeng-qing WANGJie YINXiao-tan YU...
    890-901页
    查看更多>>摘要：Objective:This study aimed to design and evaluate the efficacy of pyrrolidone derivatives as potential therapeutic agents against diffuse large B-cell lymphoma(DLBCL),a common and heterogeneous malignancy of the adult lymphohematopoietic system.Given the limitations of current therapies,there is a pressing need to develop new and effective drugs for DLBCL treatment.Methods:A series of pyrrolidone derivatives were synthesized,and their antitumor activities were assessed,particularly against DLBCL cell lines.Structure-activity relationship(SAR)analysis was conducted to identify key structural components essential for activity.The most promising compound,referred to as compound 7,was selected for further mechanistic studies.The expression levels of relevant mRNA and protein were detected by RT-qPCR and Western blotting,and the expression of mitochondrial membrane potential and ROS was detected using flow cytometry for further assessment of cell cycle arrest and apoptosis.Results:The compound 7 exhibited good antitumor activity among the synthesized derivatives,specifically in DLBCL cell lines.SAR analysis highlighted the critical role of α,β-unsaturated ketones in the antitumor efficacy of these compounds.Mechanistically,compound 7 was found to induce significant DNA damage,trigger an inflammatory response,cause mitochondrial dysfunction,and disrupt cell cycle progression,ultimately leading to apoptosis of DLBCL cells.Conclusion:The compound 7 has good antitumor activity and can induce multiple cellular mechanisms leading to cancer cell death.These findings warrant further investigation of the compound 7 as a potential therapeutic agent for DLBCL.
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    Protective Effects of Berberine on Nonalcoholic Fatty Liver Disease in db/db Mice via AMPK/SIRT1 Pathway Activation

    Cheng CHENXiao-cui LIUBin DENG
    902-911页
    查看更多>>摘要：Objective:Berberine(BBR)has emerged as a promising therapeutic agent for nonalcoholic fatty liver disease(NAFLD).This study aims to elucidate the underlying molecular mechanisms.Methods:In this study,db/db mice were chosen as an animal model for NAFLD.A total of 10 healthy C57BL/6J mice and 30 db/db mice were randomly allocated to one of 4 groups:the normal control(NC)group,the diabetic control(DC)group,the Metformin(MET)therapy group,and the BBR therapy group.The total cholesterol(TC),triacylglycerol(TG),low-density lipoprotein cholesterol(LDL-c),high-density lipoprotein cholesterol(HDL-c),aspartate aminotransferase(AST)and alanine aminotransferase(ALT)levels in the serum were measured.The glutathione peroxidase(GSH-Px),glutathione(GSH),malondialdehyde(MDA),superoxide dismutase(SOD),catalase(CAT),interleukin(IL)-1β,tumor necrosis factor(TNF)-α and monocyte chemotactic protein 1(MCP-1)levels in liver tissue were measured.Hematoxylin and eosin(H&E),acid-Schiff(PAS)and TUNEL stanning was performed for histopathological analysis.Western blotting and immunohistochemistry were conducted to detect the expression levels of key proteins in the AMPK/SIRT1 pathway.Results:BBR could improve lipid metabolism,attenuate hepatic steatosis and alleviate liver injury significantly.The excessive oxidative stress,high levels of inflammation and abnormal apoptosis in db/db mice were reversed after BBR intervention.BBR clearly changed the expression of AMP-activated protein kinase(AMPK)/Sirtuin 1(SIRT1),and their downstream proteins.Conclusion:BBR could reverse NAFLD-related liver injury,likely by activating the AMPK/SIRT1 signaling pathway to inhibit oxidative stress,inflammation and apoptosis in hepatic tissue.
      原文链接:
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    Risk Factors for Mortality in Critically Ill Patients with Coagulation Abnormalities:A Retrospective Cohort Study

    Qiu-yu GUOJun PENGTi-chao SHANMiao XU...
    912-922页
    查看更多>>摘要：Objective:Coagulation abnormalities are common and prognostically significant in intensive care units(ICUs)and are associated with increased mortality.This study aimed to explore the association between the levels of coagulation markers and the risk of mortality among ICU patients with coagulation abnormalities.Methods:This retrospective study investigated patients with coagulation abnormalities in the ICU between January 2021 and December 2022.The initial point for detecting hemestatic biomarkers due to clinical assessment of coagulation abnormalities was designated day 0.Patients were followed up for 28 days,and multivariate logistic regression analysis was utilized to identify risk factors for mortality.Results:Of the 451 patients analyzed,115 died,and 336 were alive at the end of the 28-day period.Multivariate analysis revealed that elevated thrombin-antithrombin complex(TAT),tissue plasminogen activator inhibitor complex(tPAIC),prolonged prothrombin time,and thrombocytopenia were independent risk factors for mortality.For nonovert disseminated intravascular coagulation(DIC)patients,older age and thrombocytopenia were associated with increased risks of mortality,whereas elevated levels of plasmin α2-plasmin inhibitor complex(PIC)were found to be independent predictors of survival.In patients with overt DIC,elevated levels of tPAIC were independently associated w;th increased risks of mortality.Nevertheless,thrombocytopenia was independently associated with increased risks of mortality in patients with pre-DIC.Conclusion:Coagulation markers such as the TAT,tPAIC,PIC,and platelet count were significantly associated with mortality,underscoring the importance of maintaining a balance between coagulation and fibrinolysis.These findings highlight the potential for targeted therapeutic interventions based on specific coagulation markers to improve patient outcomes.
      原文链接:
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    Clinical Value of ABCB1 and PAI-1 Gene Polymorphisms in Predicting Glucocorticoid-induced Adverse Reactions in Nephrotic Syndrome Patients

    Ya-ling ZHAIShuai-gang SUNWen-hui ZHANGHui-juan TIAN...
    923-931页
    查看更多>>摘要：Objective:Glucocorticoid(GC)-induced adverse reactions(ARs)have been extensively studied due to their potential impact on patients'health.This study aimed to examine the potential correlation between two polymorphisms[adenosine triphosphate-binding cassette B1(ABCB1)C3435T and plasminogen activator inhibitor-1(PAI-1)4G/5G]and various GC-induced ARs in nephrotic syndrome(NS)patients.Methods:In this study,513 NS patients who underwent GC treatment were enrolled.Then,the patients were divided into two groups based on ABCB1 C3435T and PAI-1 4G/5G genotyping,and intergroup comparisons of clinicopathological data and GC-induced ARs were performed.Univariate and multivariate logistic analyses were subsequently conducted to identify potential risk factors for GC-induced ARs,and a nomogram was subsequently established and validated via the area under the ROC curve(AUC),calibration curve and decision curve analysis(DCA).Results:We identified ABCB1 C3435T as an independent risk factor for the development of steroid-associated avascular necrosis of the femoral head(SANFH)(OR:2.191,95％CI:1.258-3.813,P=0.006)but not as a risk factor for the occurrence of steroid diabetes mellitus(S-DM).On the other hand,PAI-1 4G/5G was identified as an independent risk factor for the development of both SANFH(OR:2.198,95％CI:1.267-3.812,P=0.005)and S-DM(OR:2.080,95％CI:1.166-3.711,P=0.013).Notably,no significant correlation was found between the two gene polymorphisms and other GC-induced ARs.In addition,two nomograms were established and validated to demonstrate strong calibration capability and clinical utility.Conclusion:Assessing ABCB1 C3435T and PAI-1 4G/5G before steroid treatment in NS patients could be useful for identifying patients at a high risk of developing SANFH and S-DM.
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    Porphyromonas gingivalis Induces Chronic Kidney Disease through Crosstalk between the NF-κB/NLRP3 Pathway and Ferroptosis in GMCs

    Xue LIChao YAODong-mei LANYan WANG...
    932-946页
    查看更多>>摘要：Objective:Porphyromonas gingivalis(P.gingivalis)is a gram-negative bacterium found in the human oral cavity and is a recognized pathogenic bacterium associated with chronic periodontitis and systemic diseases,including chronic kidney disease(CKD),but the roles and molecular mechanism of P.gingivalis in CKD pathogenesis are unclear.Methods:In this study,an animal model of oral P.gingivalis administration and glomerular mesangial cells(GMCs)cocultured with Ml-polarized macrophages and P.gingivalis supernatant were constructed.After seven weeks of P.gingivalis gavaged,peripheral blood was collected to detect the changes in renal function.By collecting the teeth and kidneys of mice,H&E staining and IHC were used to analyze the expression of periodontal inflammatory factors in mice,PAS staining was used to analyze glomerular lesions.The supernatant of macrophages was treated with 5％P.gingivalis supernatant.H&E staining,IHC,Western blot and RT-PCR were applied to analyze renal inflammatory factors,macrophage Ml polarization,NF-κB,NLRP3 and ferroptosis changes in vitro.Results:We found that oral P.gingivalis administration induced CKD in mice.P.gingivalis supernatant induced macrophage polarization and inflammatory factor upregulation,which triggered the activation of the NF-κB/NLRP3 pathway and ferroptosis in GMCs.By inhibiting the NF-κB/NLRP3 pathway and ferroptosis in GMCs,cell viability and the inflammatory response were partially alleviated in vitro.Conclusion:We demonstrated that P.gingivalis induced CKD in mice by triggering crosstalk between the NF κB/NLRP3 pathway and ferroptosis in GMCs.Overall,our study suggested that periodontitis can promote the pathogenesis of CKD in mice,which provides evidence of the importance of periodontitis therapy in the prevention and treatment of CKD.
      原文链接:
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    Diagnostic Value of Targeted Next-generation Sequencing in Pulmonary Mycobacterial Infections

    Yu TAOZi-wei ZHOUYi-fei DUANJian-miao WANG...
    947-953页
    查看更多>>摘要：Objective:This study aimed to explore the diagnostic value of novel technique-targeted next-generation sequencing(tNGS)of bronchoalveolar lavage fluid(BALF)in pulmonary mycobacterial infections.Methods:This retrospective study was conducted on patients who underwent bronchoscopy and tNGS,smear microscopy,and mycobacterial culture of BALF.Patients with positive Mycobacterium tuberculosis(MTB)culture or GeneXpert results were classified into the tuberculosis case group.Those diagnosed with nontuberculous mycobacteria(NTM)-pulmonary disease(NTM-PD)composed the case group of NTM-PD patients.The control group comprised patients without tuberculosis or NTM-PD.Sensitivity,specificity,and receiver operating characteristic(ROC)curves were used to evaluate the diagnostic performance.Results:For tuberculosis patients with positive mycobacterial culture results,the areas under the ROC curves(AUCs)for tNGS,GeneXpert,and smear microscopy were 0.975(95％CI:0.935,1.000),0.925(95％CI:0.859,0.991),and 0.675(95％CI:0.563,0.787),respectively.For tuberculosis patients with positive GeneXpert results,the AUCs of tNGS,culture,and smear microscopy were 0.970(95％CI:0.931,1.000),0.850(95％CI:0.770,0.930),and 0.680(95％CI:0.579,0.781),respectively.For NTM-PD,the AUCs of tNGS,culture,and smear-positive but GeneXpert-negative results were 0.987(95％CI:0.967,1.000),0.750(95％CI:0.622,0.878),and 0.615(95％CI:0.479,0.752),respectively.The sensitivity and specificity of tNGS in NTM-PD patients were 100％and 97.5％,respectively.Conclusion:tNGS demonstrated superior diagnostic efficacy in mycobacterial infection,indicating its potential for clinical application.
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    Androgen Receptor Promotes Lung Cancer Metastasis by Modifying the miR23a-3p/EPHB2 Pathway

    Yan YANGJing-wen HUANGWei-wei YU
    954-963页
    查看更多>>摘要：Objective:This study aimed to investigate the reasons behind the lower survival rates in male lung cancer patients than in female lung cancer patients.Methods:Through various techniques,such as Argonaute immunoprecipitation,luciferase assays,and ChIP,this study confirmed the positive effects of androgen receptor(AR)on lung cancer cell invasion across different in vitro cell lines and in vivo mouse models.Results:The findings suggest that AR enhanced the invasion of lung cancer cells by modifying EPHB2 signals at the protein expression level,which in turn required changes in miRNA-23a-3p.Restoring miRNA-23a-3p could counteract the intensified invasion of lung cancer cells mediated by AR.Conclusion:This study revealed that AR may facilitate the lung cancer matastasis by modulating miRNA-23a-3p/EPHB2 signaling and that targeting this signaling pathway could provide new approaches to inhibit lung cancer metastasis.
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    Suppression of miR-17 Alleviates Acute Respiratory Distress-associated Lung Fibrosis by Regulating Mfn2

    Mei-xia XUTao XUNing AN
    964-970页
    查看更多>>摘要：Objective:Acute respiratory distress syndrome(ARDS)patients currently have relatively high mortality,which is associated with early lung fibrosis.This study aimed to investigate whether miR-17 suppression could alleviate ARDS-associated lung fibrosis by regulating Mfn2.Methods:A mouse model of ARDS-related lung fibrosis was constructed via intratracheal instillation of bleomycin.The expression level of miR-17 in lung tissues was detected via quantitative real time polymerase chain reaction(qRT-PCR).In the ARDS mouse model of lung fibrosis,the mitigating effects of miR-17 interference were evaluated via tail vein injection of the miR negative control or the miR-17 antagomir.The pathological changes in the lung tissue were examined via HE staining and Masson's trichrome staining,and the underlying molecular mechanism was investigated via ELISA,qRT-PCR and Western blotting.Results:Bleomycin-induced pulmonary fibrosis significantly increased collagen deposition and the levels of hydroxyproline(HYP)and miR-17.Interfering with miR-17 significantly reduced the levels of HYP and miR-17 and upregulated the expression of Mfn2.The intravenous injection of the miR-17 antagomir alleviated lung inflammation and reduced collagen deposition.In addition,interference with miR-17 could upregulate LC3B expression,downregulate p62 expression,and improve mitochondrial structure.Conclusion:Interfering with miR-17 can improve pulmonary fibrosis in mice by promoting mitochondrial autophagy via Mfn2.
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    • NSTL
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