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生物化学与生物物理学报（英文版）
生物化学与生物物理学报（英文版）

月刊

1672-9145

021-54920956 54920955

200031

上海岳阳路319号

生物化学与生物物理学报（英文版）/Journal Acta Biochimica et Biophysica SinicaCSCD北大核心CSTPCDSCI
查看更多>>本刊创刊于1958年, 为我国最早的本学科领域内的专业性学术期刊, 由中国科学院上海生命科学研究院生物化学与细胞生物学研究所主办、中国科学院主管。 刊登生物化学、分子生物学、生物物理学及其相关领域的研究论文、研究简报、综述文章及其相关信息。
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    Unraveling the metabolic potential of biocontrol fungi through omics data:a key to enhancing large-scale application strategies

    Haolin YangXiuyun WuCaiyun SunLushan Wang...
    825-832页
    查看更多>>摘要：Biological control of pests and pathogens has attracted much attention due to its green,safe and effective char-acteristics.However,it faces the dilemma of insignificant effects in large-scale applications.Therefore,an in-depth exploration of the metabolic potential of biocontrol fungi based on big omics data is crucial for a comprehensive and systematic understanding of the specific modes of action operated by various biocontrol fungi.This article analyzes the preferences for extracellular carbon and nitrogen source degradation,secondary metabolites(nonribosomal peptides,polyketide synthases)and their product characteristics and the conversion relationship between extra-cellular primary metabolism and intracellular secondary metabolism for eight different filamentous fungi with characteristics appropriate for the biological control of bacterial pathogens and phytopathogenic nematodes.Further clarification is provided that Paecilomyces lilacinus,encoding a large number of hydrolase enzymes capable of degrading pathogen protection barrier,can be directly applied in the field as a predatory biocontrol fungus,whereas Trichoderma,as an antibiosis-active biocontrol control fungus,can form dominant strains on preferred substrates and produce a large number of secondary metabolites to achieve antibacterial effects.By clarifying the levels of biological control achievable by different biocontrol fungi,we provide a theoretical foundation for their application to cropping habitats.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Salidroside ameliorates acute liver transplantation rejection in rats by inhibiting neutrophil extracellular trap formation

    Xiaoyan QinHan WangQi LiDingheng Hu...
    833-843页
    查看更多>>摘要：Acute rejection is an important factor affecting the survival of recipients after liver transplantation.Salidroside has various properties,including anti-inflammatory,antioxidant,and hepatoprotective properties.This study aims to investigate whether salidroside can prevent acute rejection after liver transplantation and to examine the under-lying mechanisms involved.An in vivo acute rejection model is established in rats that are pretreated with tacro-limus(1 mg/kg/d)or salidroside(10 or 20 mg/kg/d)for seven days after liver transplantation.In addition,an in vitro experiment is performed using neutrophils incubated with salidroside(1,10,50 or 100 μM).Hematoxylin-eosin staining,terminal deoxynucleotidyl transferase dUTP nick-end labeling staining,immunosorbent assays,im-munofluorescence analysis,Evans blue staining,and western blot analysis are performed to examine the impact of salidroside on NET formation and acute rejection in vitro and in vivo.We find that Salidroside treatment reduces pathological liver damage,serum aminotransferase level,and serum levels of IL-1β,IL-6,and TNF-α in vivo.The expressions of proteins associated with the HMGB1/TLR-4/MAPK signaling pathway(HMGB1,TLR-4,p-ERK1/2,p-JNK,p-P38,cleaved caspase-3,cleaved caspase-9,Bcl-2,Bax,IL-1β,TNF-α,and IL-6)are also decreased after salidroside treatment.In vitro experiments show that the release of HMGB1/TLR-4/MAPK signaling pathway-as-sociated proteins from neutrophils treated with lipopolysaccharide is decreased by salidroside.Moreover,sali-droside inhibits NETosis and protects against acute rejection by regulating the HMGB1/TLR-4/MAPK signaling pathway.Furthermore,salidroside combined with tacrolimus has a better effect than either of the other treatments alone.In summary,salidroside can prevent acute liver rejection after liver transplantation by reducing neutrophil extracellular trap development through the HMGB1/TLR-4/MAPK signaling pathway.
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    Lycium barbarum polysaccharide ameliorates the accumulation of lipid droplets in adipose tissue via an ATF6/SIRT1-dependent mechanism

    Rui ZhouYajing LiuWeiqian HuJing Yang...
    844-856页
    查看更多>>摘要：Lipid droplets(LDs)are dynamic organelles that store neutral lipids and are closely linked to obesity.Previous studies have suggested that Lycium barbarum polysaccharide(LBP)supplements can ameliorate obesity,but the underlying mechanisms remain unclear.In this study,we hypothesize that LBP alleviates LD accumulation in adipose tissue(AT)by inhibiting fat-specific protein 27(Fsp27)through an activating transcription factor-6(ATF6)/small-molecule sirtuin 1(SIRT1)-dependent mechanism.LD accumulation in AT is induced in high-fat diet(HFD)-fed mice,and differentiation of 3T3-L1 preadipocytes(PAs)is induced.The ability of LBP to alleviate LD accumulation and the possible underlying mechanism are then investigated both in vivo and in vitro.The influences of LBP on the expressions of LD-associated genes(ATF6 and Fsp27)are also detected.The results show that HFD and PA dif-ferentiation markedly increase LD accumulation in ATs and adipocytes,respectively,and these effects are markedly suppressed by LBP supplementation.Furthermore,LBP significantly activates SIRT1 and decreases ATF6 and Fsp27 expressions.Interestingly,the inhibitory effects of LBP are either abolished or exacerbated when ATF6 is over-expressed or silenced,respectively.Furthermore,SIRT1 level is transcriptionally regulated by LBP through opposite actions mediated by ATF6.Collectively,our findings suggest that LBP supplementation alleviates obesity by ameliorating LD accumulation,which might be partially mediated by an ATF6/SIRT1-dependent mechanism.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Activation of angiogenin expression in macrophages by lipopolysaccharide via the TLR4/NF-κB pathway in colitis

    Zhengrong YaoRongpan BaiWei LiuYaxing Liu...
    857-865页
    查看更多>>摘要：Inflammatory bowel disease(IBD)is a debilitating condition that can lead to life-threatening complications.Mac-rophages are crucial in IBD management because they secrete various cytokines and regulate tissue repair.Mac-rophage-derived angiogenin(ANG)has been shown to be essential for limiting colonic inflammation,but its upstream regulatory pathway and role in macrophages remain unclear.Here we show that ANG expression is up-regulated in macrophages during colitis treatment or upon lipopolysaccharides(LPS)treatment.Mechanistically,LPS activates Toll-like receptor 4(TLR4)to initiate NF-κB translocation from the cytoplasm to the nucleus,where it binds to the ANG promoter and enhances its transcriptional activity,leading to increased ANG expression.Inter-estingly,our data also reveal that the deletion of ANG in macrophages has no adverse effect on key macrophage functions,such as phagocytosis,chemotaxis,and cell survival.Our findings establish a"LPS-TLR4-NF-κB-ANG"regulatory axis in inflammatory disorders and confirm that ANG controls inflammation in a paracrine manner,highlighting the importance of ANG as a key mediator in the complex network of inflammatory processes.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Prostate cancer-associated transcript 6(PCAT6)promotes epithelial-mesenchymal transition and stemness and worsens prognosis in patients with colorectal cancer

    Xun SunYitao YuanSuyao LiLu Gan...
    866-878页
    查看更多>>摘要：Approximately 20％of colorectal cancer(CRC)patients are first diagnosed with metastatic colorectal cancer(mCRC)because they develop symptoms at an advanced stage.Despite advancements in treatment,patients with meta-static disease still experience inferior survival rates.Our objective is to investigate the association between long noncoding RNAs(IncRNAs)and prognosis and to explore their role in mCRC.In this study,we find that elevated expression of PCAT6 is independently linked to unfavourable survival outcomes in The Cancer Genome Atlas(TCGA)data,and this finding is further confirmed in CRC samples obtained from Fudan University Shanghai Cancer Center.Cell lines and xenograft mouse models are used to examine the impact of PCAT6 on tumor metastasis.Knockdown of PCAT6 is observed to impede the metastatic phenotype of CRC,as evidenced by functional assays,demonstrating the suppression of epithelial-mesenchymal transition(EMT)and stemness.Our findings show the significance of PCAT6 in mCRC and its potential use as a prognostic biomarker.
      原文链接:
    • NETL
    • NSTL
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    A subunit vaccine based on Brucella rBP26 induces Th1 immune responses and M1 macrophage activation

    Jia WenZihua LiYongxue LvShuqin Ding...
    879-891页
    查看更多>>摘要：Brucellosis is a global zoonotic infection caused by Brucella bacteria,which poses a significant burden on society.While transmission prevention is currently the most effective method,the absence of a licenced vaccine for humans necessitates the urgent development of a safe and effective vaccine.Recombinant protein-based subunit vaccines are considered promising options,and in this study,the Brucella BP26 protein is expressed using prokaryotic expression systems.The immune responses are evaluated using the well-established adjuvant CpG-ODN.The results demonstrate that rBP26 supplemented with a CpG adjuvant induces M1 macrophage polarization and stimulates cellular immune responses mediated by Th1 cells and CD8+T cells.Additionally,it generates high levels of rBP26-specific antibodies in immunized mice.Furthermore,rBP26 immunization activates,proliferates,and produces cytokines in T lymphocytes while also maintaining immune memory for an extended period of time.These findings shed light on the potential biological function of rBP26,which is crucial for understanding brucellosis pathogenesis.Moreover,rBP26 holds promise as an effective subunit vaccine candidate for use in endemic areas.
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    • NETL
    • NSTL
    • 万方数据

    FGF21 overexpression alleviates VSMC senescence in diabetic mice by modulating the SYK-NLRP3 inflammasome-PPARy-catalase pathway

    Yanyan HengWei WeiLinzhong ChengFeifei Wu...
    892-904页
    查看更多>>摘要：Diabetes accelerates vascular senescence,which is the basis for atherosclerosis and stiffness.The activation of the NOD-like receptor family pyrin domain containing 3(NLRP3)inflammasome and oxidative stress are closely as-sociated with progressive senescence in vascular smooth muscle cells(VSMCs).The vascular protective effect of FGF21 has gradually gained increasing attention,but its role in diabetes-induced vascular senescence needs further investigation.In this study,diabetic mice and primary VSMCs are transfected with an FGF21 activation plasmid and treated with a peroxisome proliferator-activated receptor y(PPARγ)agonist(rosiglitazone),an NLRP3 inhibitor(MCC950),and a spleen tyrosine kinase(SYK)-specific inhibitor,R406,to detect senescence-associated markers.We find that FGF21 overexpression significantly restores the level of catalase(CAT),vascular relaxation,inhibits the intensity of ROSgreen fluorescence and p21 immunofluorescence,and reduces the area of SA-β-gal staining and collagen deposition in the aortas of diabetic mice.FGF21 overexpression restores CAT,inhibits the expression of p21,and limits the area of SA-β-gal staining in VSMCs under high glucose conditions.Mechanistically,FGF21 inhibits SYK phosphorylation,the production of the NLRP3 dimer,the expression of NLRP3,and the colocalization of NLRP3 with PYCARD(ASC),as well as NLRP3 with caspase-1,to reverse the cleavage of PPARγ,preserve CAT levels,suppress ROSgreen density,and reduce the expression of p21 in VSMCs under high glucose conditions.Our results suggest that FGF21 alleviates vascular senescence by regulating the SYK-NLRP3 inflammasome-PPARγ-catalase pathway in diabetic mice.
      原文链接:
    • NETL
    • NSTL
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    Gallic acid attenuates LPS-induced inflammation in Caco-2 cells by suppressing the activation of the NF-κB/MAPK signaling pathway

    Chu ChuHuan RuYuyan ChenJinhua Xu...
    905-915页
    查看更多>>摘要：Inflammatory bowel disease(IBD)is a chronic inflammatory disease characterized by intestinal barrier dysfunction,inflammatory synergistic effects and excessive tissue injury.Gallic acid(GA)is renowned for its remarkable bio-logical activity,encompassing anti-inflammatory and antioxidant properties.However,the underlying mechanisms by which GA protects against intestinal inflammation have not been fully elucidated.The aim of this study is to investigate the effect of GA on the inflammation of a lipopolysaccharide(LPS)-stimulated human colon carcinoma cell line(Caco-2)and on the intestinal barrier dysfunction,and explore the underlying molecular mechanism involved.Our findings demonstrate that 5 µg/mL GA restores the downregulation of the mRNA and protein levels of Claudin-1,Occludin,and ZO-1 and decreases the expressions of inflammatory factors such as IL-6,IL-1β and TNF-αinduced by LPS.In addition,GA exhibits a protective effect by reducing the LPS-enhanced early and late apoptotic ratios,downregulating the mRNA levels of pro-apoptotic factors(Bax,Bad,Caspase-3,Caspase-8,and Caspase-9),and upregulating the mRNA levels of anti-apoptotic factor Bcl-2 in Caco-2 cells.GA also reduces the levels of reactive oxygen species increased by LPS and restores the activity of antioxidant enzymes,namely,superoxide dismutase and catalase,as well as the level of glutathione.More importantly,GA exerts its anti-inflammatory effects by inhibiting the LPS-induced phosphorylation of key signaling molecules in the NF-κB/MAPK pathway,including p65,IκB-α,p38,JNK,and ERK,in Caco-2 cells.Overall,our findings show that GA increases the expres-sions of tight junction proteins,reduces cell apoptosis,relieves oxidative stress and suppresses the activation of the NF-κB/MAPK pathway to reduce LPS-induced intestinal inflammation in Caco-2 cells,indicating that GA has po-tential as a therapeutic agent for intestinal inflammation.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    UBE2C enhances temozolomide resistance by regulating the expression of p53 to induce aerobic glycolysis in glioma

    Kun ZhouDexin WangXiaolin DuXia Feng...
    916-926页
    查看更多>>摘要：UBE2C is overexpressed in gliomas,and its overexpression has been reported to be correlated with the drug resistance of gliomas to some extent.In this study,we explore the role of UBE2C in regulating temozolomide(TMZ)resistance in glioma and investigate the underlying mechanisms involved.Twenty normal brain tissues and 100 glioma tissues from 50 TMZ-resistant patients and 50 TMZ-sensitive patients are included in this study.TMZ-resistant cell lines are constructed to explore the role of UBE2C in regulating glioma cell viability and TMZ re-sistance.Our results show that both the mRNA and protein levels of UBE2C are significantly elevated in the brain tissues of glioma patients,especially in those of TMZ-resistant patients.Consistently,UBE2C expression is mark-edly upregulated in TMZ-resistant cell lines.Overexpression of UBE2C rescues glioma cells from TMZ-mediated apoptosis and enhances cell viability.In contrast,downregulation of UBE2C expression further enhances TMZ function,increases cell apoptosis and decreases cell viability.Mechanistically,UBE2C overexpression decreases p53 expression and enhances aerobic glycolysis level by increasing ATP level,lactate production,and glucose uptake.Downregulation of p53 level abolishes the role of UBE2C downregulation in inhibiting TMZ resistance and aerobic glycolysis in glioma cells.Moreover,an animal assay confirms that downregulation of UBE2C expression further suppresses tumor growth in the context of TMZ treatment.Collectively,this study reveals that down-regulation of UBE2C expression enhances the sensitivity of glioma cells to TMZ by regulating the expression of p53 to inhibit aerobic glycolysis.
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    • NETL
    • NSTL
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    circlARS:a potential plasma biomarker for diagnosing non-small cell lung cancer

    Qi ZhangXinfeng FanXinyu ZhangShaoqing Ju...
    927-936页
    查看更多>>摘要：Non-small cell lung cancer(NSCLC)is one of the most prevalent cancers in the world,and early diagnosis can effectively improve patient survival.Here,differentially expressed circlARS genes are screened from the sequen-cing results,and their molecular characteristics are examined by Sanger sequencing,RNase R assay,agarose gel electrophoresis(AGE),and fluorescence in situ hybridization(FISH).Real-time fluorescence quantitative poly-merase chain reaction(qRT-PCR)is performed to detect the expression level of circlARS.The diagnostic value of the signature is analyzed using a subject operating characteristic(ROC)curve.Moreover,plasma is collected from postsurgical,chemotherapy,and relapse patients to investigate the prognostic value of circlARS in NSCLC.The expression of circlARS is greater in both the plasma and tissues of NSCLC patients than in those of healthy individuals,and could be used to distinguish NSCLC patients from patients with benign pulmonary disease(BPD),small cell lung cancer(SCLC)patients,and healthy individuals.The expression level of circlARS relatively decreases after antitumor therapy,such as chemotherapy,and relatively increases after recurrence.ROC analysis reveals that circIARS has better detection efficiency than traditional markers.In addition,circlARS expression level is strongly correlated with several clinicopathological parameters.Finally,we tentatively predict the downstream miRNAs or RBP that might bind to circlARS.Plasma circlARS is significantly greater in NSCLC patients and has good stability and specificity as a diagnostic marker,which could aid in the adjuvant diagnosis and dynamic monitoring of NSCLC.
      原文链接:
    • NETL
    • NSTL
    • 万方数据