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Based on oxidative stress of dinotefuran in SH-SY5Y cells:Chirality in energy metabolism 认领 引用 被引量：1
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作者 Jingtong Yu Yuan Tang +3 位作者 Chang Liu Aiqi Feng Quan Zhang Meirong Zhao 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第5期492-500,共9页
Dinotefuran is a widely used neonicotinoid insecticide with a chiral structure,and its potential neurotoxic mechanism has not been fully elucidated.This study revealed that S-dinotefuran showed more significant inhibi... Dinotefuran is a widely used neonicotinoid insecticide with a chiral structure,and its potential neurotoxic mechanism has not been fully elucidated.This study revealed that S-dinotefuran showed more significant inhibitory effect than R-dinotefuran and rac-(±)-dinotefuran on various mitochondrial damage indexes of SH-SY5Y.This discovery provides a new perspective for the study of the toxicity mechanism of dinotefuran.S-dinotefuran exerts cytotoxicity by suppressing the cellular antioxidant system,disrupting mitochondrial membrane potential,and interfering with energy metabolism pathways.The primary mechanism involves strong inhibition of mitochondrial respiratory chain complex activity,leading to impaired Adenosine triphosphate(ATP)synthesis and abnormal alterations in energy-related metabolites in SH-SY5Y cells. 展开更多
关键词 Neonicotinoid pesticides Dinotefuran Chirality Energy metabolism Oxidative stress SH-SY5Y cells
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miR-100-5p Enhances Cell Cycle-Mediated Chemoresistance by Modulating the CTDSPL/pRB/E2F1 Signaling Pathway in Oxaliplatin-Resistant Colorectal Cancer Cells 认领 引用
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作者 Yen-Pin Chen Rathinasamy Baskaran +12 位作者 Hema Sri Devi Chaouhan Hitesh Singh Yu-Jung Lin Marthandam Asokan Shibu Wei-Wen Kuo Shih-Chieh Liao Ming-Cheng Chen Tso-Fu Wang Chi-Cheng Li Tsung-Jung Ho Tzu-Ching Shih Shinn-Zong Lin Chih-Yang Huang 《Oncology Research》 SCIE 2026年第4期443-464,共22页
Objective:MicroRNAs(miRNAs)are small,non-coding RNAs that play a key role in the development of chemoresistance in various cancer types,including colorectal cancer(CRC).In this study,we aimed to study the underlying m... Objective:MicroRNAs(miRNAs)are small,non-coding RNAs that play a key role in the development of chemoresistance in various cancer types,including colorectal cancer(CRC).In this study,we aimed to study the underlying mechanisms of miRNA in chemotherapy-resistant CRC.Methods:LoVo CRC cell line was exposed to oxaliplatin at an increased dose,and cells were cultured in the presence of oxaliplatin to develop LoVoOXR cells.Microarray and Quantitative Reverse Transcription Polymerase Chain Reaction(qRT-PCR),western blot,and transwell assay were used to evaluate the chemoresistance in LoVoOXR CRC cells.Results:Microarray and qRT-PCR analysis showed an increased expression of miR-100-5p in LoVoOXR cells.MTT assay and flow cytometry analysis revealed less apoptosis and higher cell viability in LoVoOXR cells.mRNA prediction target gene analysis showed C-terminal domain small phosphatase-like(CTDSPL),a phosphatase-like tumor suppressor,as a key target of miR-100-5p.CTDSPL expression was low in LoVoOXR cells compared to LoVoWT cells.miR-100-5p regulates G1/S and S-phase transitions and inhibits differentiation by targeting the CTDSPL/pRB/E2F1 signaling pathway,which involves the modulation of cell cycle effectors in LoVoOXR cells.Further,we found that forkhead box P3(FOXP3),as the upstream target of miR-100-5p,is highly expressed in LoVoOXR cells.Inhibiting miR-100-5p and FOXP3 down-regulates miR-100-5p expression,while increased CTDSPL expression contributed to reduced cell proliferation and promoted cell apoptosis in LoVoOXR CRC cells.Conclusions:miR-100-5p plays an oncogenic role in inducing chemoresistance through modulation of the CTDSPLetinoblastoma protein(pRB)/E2F transcription factor 1(E2F1)axis in CRC cells. 展开更多
关键词 miR-100-5p C-terminal domain small phosphatase-like(CTDSPL)etinoblastoma protein(pRB)/E2F transcription factor 1(E2F1) chemoresistance cell cycle progression colorectal cancers
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Lidocaine Regulates the Proliferation and Apoptosis of Colorectal Cancer Cells by Modulating AKR1B1/miR-21-5p Pathway 认领 引用
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作者 Luyao Wang Jie Zhou +4 位作者 Hui Yang Lulu Shen Wenzhuang Zheng Lei Wang Chenglan Xie 《Proceedings of Anticancer Research》 2026年第3期1-11,共11页
This study was to investigate the effect of lidocaine on the proliferation and apoptosis of the human colorectal carcinoma cell line(HCT116)and explore the underlying mechanism.HCT116 cells’proliferation and apoptosi... This study was to investigate the effect of lidocaine on the proliferation and apoptosis of the human colorectal carcinoma cell line(HCT116)and explore the underlying mechanism.HCT116 cells’proliferation and apoptosis rate were determined by CCK8 assay and flow cytometry,followed by treating the cells with 0.5 mM and 1 mM lidocaine.HCT116 cells were transfected with NC-mimic,Mimic-miR-21-5p,inhibitor-NC,and Inhibitor-miR-21-5p,followed by treatment with Lidocaine and fidarestat,combined and both alone.The expression of miR-21-5p and of AKR1B1,PTEN,p-AKT,AKT,and PI3K proteins was determined by qRT-PCR and Western blot.This study find lidocaine inhibited cell proliferation and promoted apoptosis in a time-dose dependent manner.Lidocaine and fidarestat,both alone and in combination,reduced the expression of miR-21-5p and AKR1B1.Lidocaine and fidarestat alone and combined treatments and the miR-21-5p-inhibitor group decreased the expression of p-AKT and PI3K and vice versa in the mimic-miR-21-5p group.The expression of PTEN was increased in the lidocaine+fidarestat group,decreased in the mimic-miR-21-5p group.These results suggest that lidocaine inhibited the proliferation of HCT116 cells and promoted cell apoptosis by downregulating the expression of AKR1B1/miR-21-5p and further modulating the PTEN/AKT/PI3K signaling pathway. 展开更多
关键词 Colorectal cancer Lidocaine Cell proliferation Apoptosis miR-21-5p AKR1B1
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Isoliquiritigenin Suppresses Oral Squamous Cell Carcinoma Progression by Targeting FABP5-Mediated Lipid Metabolism:Association with the circPOLB/miR-548ae-3p/C-MYC Axis 认领 引用
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作者 Liang Li Hong Deng +4 位作者 Zhiyong Li Yu Li Lingrui Liu Lan Xie Yue Chen 《Oncology Research》 SCIE 2026年第8期590-604,共15页
Objectives:Oral squamous cell carcinoma(OSCC)is a common and deadly cancer affecting the oral cavity.This study aims to explore the regulatory role and molecular mechanism of miR-548ae-3p in OSCC proliferation,invasio... Objectives:Oral squamous cell carcinoma(OSCC)is a common and deadly cancer affecting the oral cavity.This study aims to explore the regulatory role and molecular mechanism of miR-548ae-3p in OSCC proliferation,invasion,and lipid metabolism,as well as the therapeutic potential of isoliquiritigenin(ISL)targeting OSCC lipid metabolism.Methods:Expression levels of miR-548ae-3p were measured in OSCC cell lines and normal oral keratinocytes using real-time quantitative polymerase chain reaction.Functional assays,such as cell counting Kit-8 proliferation and Transwell invasion assays,evaluated the effects of miR-548ae-3p overexpression in CAL-27 and SCC-25 cells.Bioinformatic prediction and dual-luciferase reporter assays investigated interactions among miR-548ae-3p,hsa_circRNA_0001794(circPOLB),and cellular myelocytomatosis oncogene(c-MYC).Lipid metabolism was assessed using lipid droplet staining,fatty acid oxidation assays,total fatty acids and palmitic acid quantification,and fatty acid-binding protein 5(FABP5)expression analysis.The inhibitory effects of ISL on OSCC lipid metabolism and invasiveness were also examined.Results:MiR-548ae-3p was downregulated in OSCC cells compared to normal keratinocytes(n=3,p<0.001).miR-548ae-3p overexpression inhibited the proliferation and invasion of CAL-27 and SCC-25 cells(n=3,p<0.001).CircPOLB functions as a molecular sponge for miR-548ae-3p,which in turn targets c-MYC,a key oncogene.MiR-548ae-3p overexpression reduced lipid droplet accumulation,fatty acid oxidation,total fatty acid content,and intracellular palmitic acid levels,accompanied by downregulation of FABP5(n=3,p<0.001).Furthermore,ISL treatment decreased FABP5 expression,fatty acid metabolism,and invasive capacity of OSCC cells(n=3,p<0.001),supporting its potential as a therapeutic agent.Conclusions:MiR-548ae-3p displays tumorsuppressive activity in OSCC,restraining proliferation,invasion,and fatty-acid metabolism through engagement of the circPOLB/c-MYC axis and is associated with reduced FABP5 expression.Targeting lipid metabolism using agents like ISL could be a promising approach for treating OSCC. 展开更多
关键词 Oral squamous cell carcinoma miR-548ae-3p c-MYC circPOLB FABP5
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Small extracellular vesicles derived from hair follicle neural crest stem cells enhance perineurial cell proliferation and migration via the TGF-β/SMAD/HAS2 pathway 认领 引用
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作者 Yiming Huo Bing Xiao +8 位作者 Haojie Yu Yang Xu Jiachen Zheng Chao Huang Ling Wang Haiyan Lin Jiajun Xu Pengfei Yang Fang Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第5期2060-2072,共13页
Peripheral nerve defect repair is a complex process that involves multiple cell types;perineurial cells play a pivotal role.Hair follicle neural crest stem cells promote perineurial cell proliferation and migration vi... Peripheral nerve defect repair is a complex process that involves multiple cell types;perineurial cells play a pivotal role.Hair follicle neural crest stem cells promote perineurial cell proliferation and migration via paracrine signaling;however,their clinical applications are limited by potential risks such as tumorigenesis and xenogeneic immune rejection,which are similar to the risks associated with other stem cell transplantations.The present study therefore focuses on small extracellular vesicles derived from hair follicle neural crest stem cells,which preserve the bioactive properties of the parent cells while avoiding the transplantation-associated risks.In vitro,small extracellular vesicles derived from hair follicle neural crest stem cells significantly enhanced the proliferation,migration,tube formation,and barrier function of perineurial cells,and subsequently upregulated the expression of tight junction proteins.Furthermore,in a rat model of sciatic nerve defects bridged with silicon tubes,treatment with small extracellular vesicles derived from hair follicle neural crest stem cells resulted in higher tight junction protein expression in perineurial cells,thus facilitating neural tissue regeneration.At 10 weeks post-surgery,rats treated with small extracellular vesicles derived from hair follicle neural crest stem cells exhibited improved nerve function recovery and reduced muscle atrophy.Transcriptomic and micro RNA analyses revealed that small extracellular vesicles derived from hair follicle neural crest stem cells deliver mi R-21-5p,which inhibits mothers against decapentaplegic homolog 7 expression,thereby activating the transforming growth factor-β/mothers against decapentaplegic homolog signaling pathway and upregulating hyaluronan synthase 2 expression,and further enhancing tight junction protein expression.Together,our findings indicate that small extracellular vesicles derived from hair follicle neural crest stem cells promote the proliferation,migration,and tight junction protein formation of perineurial cells.These results provide new insights into peripheral nerve regeneration from the perspective of perineurial cells,and present a novel approach for the clinical treatment of peripheral nerve defects. 展开更多
关键词 hair follicle neural crest stem cells HAS2 migration miR-21-5p perineurial cells proliferation peripheral nerve injury Smad7 small extracellular vesicles transforming growth factor-β/SMAD signaling pathway
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Nicotinamide mononucleotide protects against diabetic nephropathy via IL-6/Rab5-mediated crosstalk between proximal tubular epithelial cells and podocytes 认领 引用 被引量：2
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作者 Dong-Qing Zha Ping Gao Xiao-Yan Wu 《World Journal of Diabetes》 SCIE 2025年第10期324-343,共20页
BACKGROUND Diabetic nephropathy(DN)is a leading cause of chronic kidney disease and endstage renal disease,and is a significant global healthcare burden.Although proximal tubular epithelial cells(PTECs)and podocytes a... BACKGROUND Diabetic nephropathy(DN)is a leading cause of chronic kidney disease and endstage renal disease,and is a significant global healthcare burden.Although proximal tubular epithelial cells(PTECs)and podocytes are involved in DN progression,the specific molecular interactions between these cells are not well understood.AIM To elucidate the role of interleukin-6(IL-6)/Rab5 signaling in mediating crosstalk between PTECs and podocytes,and to evaluate the protective effects of nicotinamide mononucleotide(NMN)against DN progression.METHODS We utilized in vitro and in vivo models to investigate the pathogenesis of DN.In vitro,human PTECs and murine podocytes were cultured under high-glucose conditions,and IL-6 neutralizing antibodies or NMN treatments were applied.Podocyte injury was assessed by measurements of nephrin endocytosis,Rab5 activity,cytoskeletal organization,cell adhesion,and cell-spreading assays.In vivo,DN was induced in mice using streptozotocin,and mice then received NMN,insulin,or both treatments over an 8-week period.Renal tissues were analyzed histologically,ultrastructurally,and immunochemically,and urinary albumin excretion was measured to assess renal function.Statistical analyses were conducted using one-way ANOVA and Tukey's test.RESULTS High-glucose conditions induced the epithelial-mesenchymal transition(EMT)in PTECs,increased IL-6 secretion,and activated Rab5 signaling in podocytes,leading to increased nephrin endocytosis and podocyte injury.Blocking IL-6 significantly attenuated these effects.NMN treatment of diabetic mice markedly reduced podocyte injury,glomerular hypertrophy,foot-process effacement,and urinary albumin excretion.Mechanistically,NMN suppressed the EMT and IL-6 secretion by PTECs,inhibited Rab5 activation in podocytes,and prevented nephrin endocytosis,thereby preserving the cytoskeletal integrity and function of podocytes.CONCLUSION Our findings reveal a novel pathogenic mechanism of DN in which IL-6 released from glucose-stressed PTECs activates Rab5 signaling in podocytes,followed by nephrin endocytosis and structural injury of podocytes.Importantly,NMN treatment effectively disrupted this pathological pathway of intercellular communication,and provided significant protection against DN progression.These results suggest that NMN supplementation and targeting the IL-6/Rab5 signaling axis has promise as a therapeutic strategy for managing DN. 展开更多
关键词 Diabetic nephropathy Podocyte injury Interleukin-6 Rab5 signaling Nicotinamide mononucleotide Proximal tubular epithelial cell
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Gamma-glutamyl transferase 5 overexpression in cerebrovascular endothelial cells improves brain pathology,cognition,and behavior in APP/PS1 mice 认领 引用
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作者 Yanli Zhang Tian Li +8 位作者 Jie Miao Zhina Zhang Mingxuan Yang Zhuoran Wang Bo Yang Jiawei Zhang Haiting Li Qiang Su Junhong Guo 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第2期533-547,共15页
In patients with Alzheimer’s disease,gamma-glutamyl transferase 5(GGT5)expression has been observed to be downregulated in cerebrovascular endothelial cells.However,the functional role of GGT5 in the development of A... In patients with Alzheimer’s disease,gamma-glutamyl transferase 5(GGT5)expression has been observed to be downregulated in cerebrovascular endothelial cells.However,the functional role of GGT5 in the development of Alzheimer’s disease remains unclear.This study aimed to explore the effect of GGT5 on cognitive function and brain pathology in an APP/PS1 mouse model of Alzheimer’s disease,as well as the underlying mechanism.We observed a significant reduction in GGT5 expression in two in vitro models of Alzheimer’s disease(Aβ1-42-treated hCMEC/D3 and bEnd.3 cells),as well as in the APP/PS1 mouse model.Additionally,injection of APP/PS1 mice with an adeno-associated virus encoding GGT5 enhanced hippocampal synaptic plasticity and mitigated cognitive deficits.Interestingly,increasing GGT5 expression in cerebrovascular endothelial cells reduced levels of both soluble and insoluble amyloid-βin the brains of APP/PS1 mice.This effect may be attributable to inhibition of the expression ofβ-site APP cleaving enzyme 1,which is mediated by nuclear factor-kappa B.Our findings demonstrate that GGT5 expression in cerebrovascular endothelial cells is inversely associated with Alzheimer’s disease pathogenesis,and that GGT5 upregulation mitigates cognitive deficits in APP/PS1 mice.These findings suggest that GGT5 expression in cerebrovascular endothelial cells is a potential therapeutic target and biomarker for Alzheimer’s disease. 展开更多
关键词 Alzheimer’s disease amyloid-β APP/PS1 mice cerebrovascular endothelial cells cognitive deficits gamma-glutamyl transferase 5 neurovascular unit nuclear factor‐kappa B synaptic plasticity β-site APP cleaving enzyme 1
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用于狂犬病疫苗生产的MRC-5工作细胞库的建立及相关研究 认领 引用
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作者 左静 赵鹭 +5 位作者 马春岭 资静 程超 刘勇 张伟业 佟巍 《生物技术进展》 CAS 2026年第1期164-169,共6页
研究旨在建立医学研究委员会5号细胞系(medical research council 5,MRC-5)工作细胞库,并对MRC-5工作细胞库应用于狂犬病灭活疫苗的生产进行相关研究。按照《中华人民共和国药典》建立MRC-5工作细胞库,根据药典规定进行检验,并对MRC-5... 研究旨在建立医学研究委员会5号细胞系(medical research council 5,MRC-5)工作细胞库,并对MRC-5工作细胞库应用于狂犬病灭活疫苗的生产进行相关研究。按照《中华人民共和国药典》建立MRC-5工作细胞库,根据药典规定进行检验,并对MRC-5细胞生长曲线、传代稳定性及狂犬病病毒适应性进行研究。结果表明,建立的MRC-5细胞工作库细胞呈长梭形,边缘清晰,轮廓清楚,细胞成活率为99.03%,无菌检查、支原体检查及细胞外源因子检查均符合规定。MRC-5细胞生长曲线呈S形,细胞在2~3 d进入对数生长期,细胞倍增时间为21 h,连续传代至66代细胞形态正常。36、38、40和42代的MRC-5细胞接种PM株狂犬病病毒,测得病毒滴度均值分别为6.57±0.21、6.40±0.26、6.23±0.21和6.40±0.17lgCCID50·mL-1,变异系数(coefficient of variation,CV)在2.70%~4.13%。综上,研究建立的MRC-5工作细胞库符合《中华人民共和国药典》规定,传代稳定性良好,对狂犬病病毒较为敏感,可以用于狂犬病疫苗的生产。 展开更多
关键词 MRC-5细胞 工作细胞库 传代稳定性 狂犬病疫苗
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Icariin targets PDE5A to regulate viability,DNA synthesis and DNA damage of spermatogonial stem cells and improves reproductive capacity 认领 引用 被引量：2
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作者 Tian-Long Liao Cai-Mei He +3 位作者 Di Xiao Zhi-Rong Zhang Zuping He Xiao-Ping Yang 《Asian Journal of Andrology》 SCIE CAS CSCD 2025年第4期543-549,共7页
Icariin is a pure compound derived from Epimedium brevicornu Maxim,and it helps the regulation of male reproduction.Nevertheless,the role and underlying mechanisms of Icariin in mediating male germ cell development re... Icariin is a pure compound derived from Epimedium brevicornu Maxim,and it helps the regulation of male reproduction.Nevertheless,the role and underlying mechanisms of Icariin in mediating male germ cell development remain to be clarified.Here,we have demonstrated that Icariin promoted proliferation and DNA synthesis of mouse spermatogonial stem cells(SSCs).Furthermore,surface plasmon resonance iron(SPRi)and molecular docking(MOE)assays revealed that phosphodiesterase 5A(PDE5A)was an important target of Icariin in mouse SSCs.Mechanically,Icariin decreased the expression level of PDE5A.Interestingly,hydrogen peroxides(H2O2)enhanced the expression level of phosphorylation H2A.X(p-H2A.X),whereas Icariin diminished the expression level of p-H2A.X and DNA damage caused by H2O2 in mouse SSCs.Finally,our in vivo animal study indicated that Icariin protected male reproduction.Collectively,these results implicate that Icariin targets PDE5A to regulate mouse SSC viability and DNA damage and improves male reproductive capacity.This study thus sheds new insights into molecular mechanisms underlying the fate decisions of mammalian SSCs and offers a scientific basis for the clinical application of Icariin in male reproduction. 展开更多
关键词 DNA damage Icariin PDE5A proliferation spermatogonial stem cells
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Exosomes derived from human umbilical cord mesenchymal stem cells attenuate hepatic ischaemia-reperfusion injury via the let-7i- 5p/Faslg axis 认领 引用 被引量：1
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作者 Yao Gao Min He +6 位作者 Cong-Wen Bian Rui Yu Jia-Jiao Luo Yin-Ming Xiang Yun-Xin Yang Han-Fei Huang Zhong Zeng 《World Journal of Gastroenterology》 SCIE CAS 2025年第33期93-112,共20页
BACKGROUND Hepatic ischaemia-reperfusion injury(HIRI)is an unavoidable process in liver transplantation,where apoptosis plays a critical role.Human umbilical cord mesenchymal stem cell-derived exosomes(hucMSC-exos),wh... BACKGROUND Hepatic ischaemia-reperfusion injury(HIRI)is an unavoidable process in liver transplantation,where apoptosis plays a critical role.Human umbilical cord mesenchymal stem cell-derived exosomes(hucMSC-exos),which constitute a cellfree therapeutic approach,have garnered extensive attention in alleviating HIRI.However,the potential of hucMSC-exos in mitigating apoptosis and their underlying mechanisms remain largely unknown.AIM To investigate the effects of hucMSC-exos on apoptosis after HIRI and explore the underlying mechanisms.METHODS The therapeutic effects of hucMSC-exos on HIRI and hypoxiaeoxygenation injury in L02 cells were investigated.RNA sequencing was used to detect differentially expressed genes in L02 cells after hucMSC-exo treatment,and the expression of apoptosis markers in L02 cells was analyzed.MicroRNA(miRNA)sequencing was performed to analyse the miRNA expression profiles of hucMSCexos and L02 cells after hucMSC-exo treatment.Through a miRNA-mRNA integrated analysis,candidate miRNAs and their regulated target genes were identified.We subsequently studied the roles of these candidate miRNAs in mouse HIRI and L02 cell hypoxiaeoxygenation injury.RESULTSFluorescence confocal microscopy revealed that hucMSC-exos effectively homed to the liver and were taken up byhepatocytes, likely due to the presence of anti-very late antigen-4 and anti-lymphocyte function-associated antigen-1 on the surface of hucMSC-exos. HucMSC-exos alleviate hepatocyte damage by inhibiting apoptosis. Specifically,let-7i-5p within hucMSC-exos inhibited the expression of the factor-related apoptosis ligand protein in L02 cells,leading to the upregulation of B-cell lymphoma-2 and the downregulation of B-cell lymphoma-2-associated Xprotein and cysteinyl aspartate specific proteinase-3, thereby inhibiting L02 cell apoptosis and enhancing cellproliferation activity. The overexpression of let-7i-5p effectively enhanced the antiapoptotic effects of hucMSC-exosboth in vitro and in vivo.CONCLUSIONOur findings indicate that hucMSC-exos alleviate HIRI by inhibiting apoptosis. We demonstrated that hucMSCexostarget apoptosis in L02 cells and mediate the let-7i-5p/factor-related apoptosis ligand pathway, therebyameliorating HIRI. This study provides new insights into the role of hucMSC-exos in hepatocyte apoptosis andhighlights the potential of hucMSC-exos as a therapeutic strategy for HIRI. 展开更多
关键词 Mesenchymal stem cells Exosomes Let-7i-5p Ischaemia-reperfusion injury Liver
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ELK1-CDKL5-Rac1 signaling pathway regulates the migration of endothelial cells to promote angiogenesis induced by nanoniobium particles 认领 引用
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作者 Xiao-He Zhou Min-Hua Mo +7 位作者 Zi-Wei Chen Wen-Jing Liu Yan-Li Zhang Janak LPathak Li-Jing Wang Chang Liu Long-Quan Shao Liang-Jiao Chen 《Rare Metals》 SCIE EI CAS CSCD 2025年第1期444-460,共17页
Promotion of angiogenesis is crucial for bone tissue repair,and the poor activity of angiogenic cells and growth factors is the main problem in angiogenesis.New proangiogenic nanomaterials are urgently needed to be a ... Promotion of angiogenesis is crucial for bone tissue repair,and the poor activity of angiogenic cells and growth factors is the main problem in angiogenesis.New proangiogenic nanomaterials are urgently needed to be a promising strategy for this issue.Nb promotes bone formation and fracture healing,possibly by increasing vascular endothelial growth factor(VEGF)production.Nanoniobium particles(nNb)may promote angiogenesis.However,the effect of nNb on angiogenesis is unclear,limiting its application.This study confirmed that nNb significantly promoted angiogenesis.nNb increased and Ras-related C3 botulinum toxin substrate(Rac)family small guanosine triphosphatase(GTPase)1(Rac1)expression,inducing F-actin aggregation at the front edge of cells and the formation of pseudopodia to mediate cell migration,further promoting angiogenesis.We discovered that cyclin-dependent kinase-like 5(CDKL5)is a new signaling molecule that activates Rac1.V-ets erythroblastosis virus E26 oncogene homolog(ETS)domain-containing protein(ELK1),regulating CDKL5 and Rac1,plays an upstream regulatory role.When ELK1 was inhibited,CDKL5 and Rac1 levels were decreased.ELK1,CDKL5 or Rac1 are effective regulatory targets of angiogenesis.Inhibiting expression of ELK1,CDKL5 or Rac1 decreased angiogenesis.Thus,nNb has good angiogenic effects.The ELK1-CDKL5-Rac1 signaling pathway regulates the migration of endothelial cells to promote angiogenesis.nNb can be used in bone tissue engineering as a new nanomaterial,and it will promote the development of a new strategy for tissue engineering. 展开更多
关键词 Nanoniobium particles Angiogenesis Endothelial cells Migration ELK1-CDKL5-Rac1 signaling pathway
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FOXP1 promotes the proliferation and self-renewal of spermatogonial stem cells via the nuclear factor kappa B pathway 认领 引用
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作者 Jin-Hua Wu Feng Lin +3 位作者 Yan-Hua Wang Jiang-Ping Xie Shu-Lin Guo Pei-Yan Liu 《World Journal of Stem Cells》 SCIE 2026年第5期113-121,共9页
BACKGROUND The proliferation and self-renewal of spermatogonial stem cells(SSCs)are essential for maintaining the sperm production process.The molecular mechanisms of self-renewal and differentiation of SSCs have not ... BACKGROUND The proliferation and self-renewal of spermatogonial stem cells(SSCs)are essential for maintaining the sperm production process.The molecular mechanisms of self-renewal and differentiation of SSCs have not been fully clarified,although the functions of some regulatory factors in SSCs have been previously reported.AIM To investigate the role of forkhead box P1(FOXP1)in regulating the proliferation and self-renewal of SSCs and its potential mechanism via the nuclear factor kappa B(NF-κB)pathway.METHODS Testicular tissue was collected from 31 patients,including 18 obstructive azoospermia(OA)and 13 nonobstructive azoospermia cases.Hematoxylin and eosin staining was performed to analyze the morphological difference in human testicular tissue between the OA and nonobstructive azoospermia groups.Immunohistochemistry staining was used to evaluate the expression of FOXP1 in human testicle tissues.FOXP1 knockdown lentivirus was injected into mice testes,and immunohistochemistry staining and immunofluorescence assays of ETS variant gene 5 and promyelocytic leukemia zinc finger were performed to investigate the effect of FOXP1 on spermatogonia in mice.A Cell Counting Kit-8 assay was used to assess the proliferation of SSCs.SC75741 was used to inhibit the NF-κB pathway,and proliferating cell nuclear antigen,ETS variant gene 5,promyelocytic leukemia zinc finger,and phosphorylated-NF-κB p65 were detected via western blot analysis.RESULTS FOXP1 was highly expressed in the testicular tissue of patients with OA.FOXP1 knockdown inhibited the proliferation and self-renewal of SSCs in mice and in vitro.Consistently,FOXP1 overexpression promoted the SSCs’proliferation and self-renewal,which was regulated through the NF-κB pathway.CONCLUSION FOXP1 may promote the proliferation and self-renewal of SSCs via the NF-κB pathway.This research offers a theoretical foundation for male infertility treatment. 展开更多
关键词 Forkhead box P1 Spermatogonial stem cells Proliferation Self-renewal Nuclear factor kappa B pathway Male infertility Azoospermia ETS variant gene 5 Promyelocytic leukemia zinc finger
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Elemene as a binding stabilizer of microRNA-145-5p suppresses the growth of non-small cell lung cancer 认领 引用 被引量：3
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作者 Meirong Zhou Jiayue Wang +12 位作者 Yulin Peng Xiangge Tian Wen Zhang Junlin Chen Yue Wang Yu Wang Youjian Yang Yongwei Zhang Xiaokui Huo Yuzhuo Wu Zhenlong Yu Tian Xie Xiaochi Ma 《Journal of Pharmaceutical Analysis》 SCIE CAS CSCD 2025年第3期585-598,共14页
Elemene is widely recognized as an effective anti-cancer compound and is routinely administered in Chinese clinical settings for the management of several solid tumors,including non-small cell lung cancer(NSCLC).Howev... Elemene is widely recognized as an effective anti-cancer compound and is routinely administered in Chinese clinical settings for the management of several solid tumors,including non-small cell lung cancer(NSCLC).However,its detailed molecular mechanism has not been adequately demonstrated.In this research,it was demonstrated that elemene effectively curtailed NSCLC growth in the patient-derived xenograft(PDX)model.Mechanistically,employing high-throughput screening techniques and subsequent biochemical validations such as microscale thermophoresis(MST),microRNA-145-5p(miR-145-5p)was pinpointed as a critical target through which elemene exerts its anti-tumor effects.Interestingly,elemene serves as a binding stabilizer for miR-145-5p,demonstrating a strong binding affinity(dissociation constant(KD)=0.39±0.17μg/mL)and preventing its degradation both in vitro and in vivo,while not interfering with the synthesis of the primary microRNA transcripts(pri-miRNAs)and precursor miRNAs(pre-miRNAs).The stabilization of miR-145-5p by elemene resulted in an increased level of this miRNA,subsequently suppressing NSCLC progression through the miR-145-5p/mitogen-activated protein kinase kinase kinase 3(MAP3K3)uclear factor kappaB(NF-κB)pathway.Our findings provide a new perspective on revealing the interaction patterns between clinical anti-tumor drugs and miRNAs. 展开更多
关键词 Elemene Inflammatory Nuclear factor kappaB microRNA-145-5p Non-small cell lung cancer
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scRNA-seq of the intestine reveals the key role of mast cells in early gut dysfunction associated with acute pancreatitis 认领 引用 被引量：2
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作者 Zu-Xing Wei Shi-He Jiang +4 位作者 Xiao-Yan Qi Yi-Miao Cheng Qiong Liu Xu-Yang Hou Jun He 《World Journal of Gastroenterology》 SCIE CAS 2025年第12期108-135,共28页
BACKGROUND Intestinal barrier dysfunction is a prevalent and varied manifestation of acute pancreatitis(AP).Molecular mechanisms underlying the early intestinal barrier in AP remain poorly understood.AIM To explore th... BACKGROUND Intestinal barrier dysfunction is a prevalent and varied manifestation of acute pancreatitis(AP).Molecular mechanisms underlying the early intestinal barrier in AP remain poorly understood.AIM To explore the biological processes and mechanisms of intestinal injury associated with AP,and to find potential targets for early prevention or treatment of intestinal barrier injury.METHODS This study utilized single-cell RNA sequencing of the small intestine,alongside in vitro and in vivo experiments,to examine intestinal barrier function homeostasis during the early stages of AP and explore involved biological processes and potential mechanisms.RESULTS Seventeen major cell types and 33232 cells were identified across all samples,including normal,AP1(4x caerulein injections,animals sacrificed 2 h after the last injection),and AP2(8x caerulein injections,animals sacrificed 4 h after the last injection).An average of 980 genes per cell was found in the normal intestine,compared to 927 in the AP1 intestine and 1382 in the AP2 intestine.B cells,dendritic cells,mast cells(MCs),and monocytes in AP1 and AP2 showed reduced numbers compared to the normal intestine.Enterocytes,brush cells,enteroendocrine cells,and goblet cells maintained numbers similar to the normal intestine,while cytotoxic T cells and natural killer(NK)cells increased.Enterocytes in early AP exhibited elevated programmed cell death and intestinal barrier dysfunction but retained absorption capabilities.Cytotoxic T cells and NK cells showed enhanced pathogen-fighting abilities.Activated MCs,secreted chemokine(C-C motif)ligand 5(CCL5),promoted neutrophil and macrophage infiltration and contributed to barrier dysfunction.CONCLUSION These findings enrich our understanding of biological processes and mechanisms in AP-associated intestinal injury,suggesting that CCL5 from MCs is a potential target for addressing dysfunction. 展开更多
关键词 Single-cell RNA sequencing Acute pancreatitis Mast cell CCL5 Intestinal barrier function
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miRNA-21-5p targeting PTEN to regulate PI3K/Akt/mTOR pathway in retinal pigment epithelial cell photodamage 认领 引用 被引量：3
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作者 Juan Li Ruo-Di Shi +2 位作者 Qing Li Chen Xu Yang Yu 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2025年第4期575-581,共7页
AIM:To highlight the importance of microRNA(miRNA)-21-5p in directing the phosphatase and tensin homolog(PTEN)gene to control the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR)... AIM:To highlight the importance of microRNA(miRNA)-21-5p in directing the phosphatase and tensin homolog(PTEN)gene to control the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR)pathway in retinal pigment epithelial(RPE)cells in humans subjected to photodamage.METHODS:Human adult RPE cell line-19(ARPE-19)was cultured in vitro and randomly divided into control,damage,overexpression,negative,and PI3K/Akt blocker groups to establish a photodamage model of ARPE-19 cells.The models were subjected to 24h of light exposure,after which the corresponding indices were detected.The cell counting kit-8 assay quantified cell viability,while flow cytometry determined apoptosis rates.The miRNA-21 mimics and miRNA mimic NC were transfected into ARPE-19 cells using a transient transfection technique.Quantitative reverse transcription polymerase chain reaction(SYBR Green)and Western blotting analyzed expression levels of miRNA-21-5p,PTEN,p-PI3K/PI3K,p-mTOR/mTOR,and p-Akt/Akt.Statistical analyses comprised one-way analysis of variance and the Student-Newman-Keuls test for multiple group comparisons.RESULTS:The photodamage group demonstrated reduced cell survival rates than the control group(P0.05).The PI3K/Akt blocker group demonstrated lower cell viability,compared with the overexpression group(P<0.01).CONCLUSION:miRNA-21-5p significantly increases ARPE-19 cell survival after photodamage and inhibits lightinduced ARPE-19 cell apoptosis,suggesting that it may play a protective role in RPE by activating the PI3K/Akt/mTOR pathway while downregulating PTEN expression. 展开更多
关键词 retinal pigment epithelial cell photodamage apoptosis PI3K/Akt/mTOR signaling pathway miRNA-21-5p
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A study on the differences of effect on mast cells and serum 5-HT in the acupoint area of "CV 4" of rats by acupuncture stimulus and thermal stimulus 认领 引用 被引量：11
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作者 Qiong LIU Wei ZHU +5 位作者 Mai-lan LIU Xia LIU Jia-nan CAO Shu-ning HU Xiao-rong CHANG Xiang-hong JING 《World Journal of Acupuncture-Moxibustion》 CAS CSCD 2018年第4期257-262,311-312,共6页
Objective: To observe the influence of acupuncture stimulus and thermal stimulus on the expression of mast cells(MCs) and 5-hydroxytryptamine(5-HT) in local acupoint area of Guanyuan(关元 CV 4) and serum 5-HT in rats.... Objective: To observe the influence of acupuncture stimulus and thermal stimulus on the expression of mast cells(MCs) and 5-hydroxytryptamine(5-HT) in local acupoint area of Guanyuan(关元 CV 4) and serum 5-HT in rats.Methods: Thirty-nine male C57 BL/6 rats were randomly divided into blank control group, acupuncture stimulus group and thermal stimulus group, with 13 rats in each group. The rats were stimulated by manual acupuncture at CV 4 for 5 min in acupuncture stimulus group, while those in thermal stimulus group were stimulated by adopting a thermal moxibustion apparatus on CV 4 for 30 min. The expression of MC and 5-HT in the skin in the acupoint area of CV 4 before and after acupuncture stimulus and thermal stimulus was observed and analyzed via adopting toluidine blue staining method and immunofluorescence histochemical method(5 rats were selected from each group), and the 5-HT content in serum before and after stimulus was determined through enzyme-linked immunosorbent assay(ELISA)(8 rats were selected from each group). The influence of acupuncture stimulus and thermal stimulus on the contents of MC and 5-HT in the skin and serum 5-HT in rats was analyzed and compared.Results: ① After acupuncture stimulus or thermal stimulus on CV 4 of C57 BL/6 rats, the number of MC in the acupoint area significantly increased when compared with that in blank group(the acupuncture stimulus group 12.40 ± 2.07 vs. the blank group 3.00 ±5.96;thermal stimulus group 26.20 ± 10.85 vs. the blank group 12.40 ± 2.07, both P< 0.05), and MC aggregation and degranulation were observed(the acupuncture stimulus group 17.80 ±4.55 vs. the blank group 8.00 ±3.16;the thermal stimulus group24.00±9.05 vs. the blank group 8.00±3.16. P<0.05, P< 0.01).② After acupuncture stimulus or thermal stimulus, 5-HT was released by MCs in the acupoint area, which aggregated around the blood vessels,and the number of 5-HT in the acupoint area significantly increased when compared with that in blank group(the blank group 3.00 ±1.28 vs. the acupuncture stimulus group 10.02 ±3.21;the blank group3.00 ±1.28 vs. the thermal stimulus group 14.00 ±3.94, both P< 0.01).③ Compared with blank group,both acupuncture stimulus and thermal stimulus could reduce the 5-HT content in serum(the blank group 0.72 ±0.2372 vs. acupuncture stimulus group 0.43 ±0.21: the blank group 0.72 ±0.24 vs. thermal stimulus group 0.32 ±0.18, both P<0.01), and the effect in thermal stimulus group was slightly superior to that in acupuncture stimulus group(P<0.05).Conclusion: Both acupuncture stimulus and thermal stimulus can cause the aggregation and degranulation of MCs and high expression of 5-HT in the acupoint area. The effect of thermal stimulus was superior to that of acupuncture stimulus in degranulation. 展开更多
关键词 Acupuncture Moxibostion Thermal stimulus Mast cell(MC) 5-hydroxytryptamine(5-HT)
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Synergistic anticancer properties of docosahexaenoic acid and 5-fluorouracil through interference with energy metabolism and cell cycle arrest in human gastric cancer cell line AGS cells 认领 引用 被引量：6
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作者 Kun Gao Qi Liang +2 位作者 Zhi-Hao Zhao You-Fen Li Shu-Feng Wang 《World Journal of Gastroenterology》 SCIE CAS 2016年第10期2971-2980,共10页
AIM: To explore the synergistic effect of docosahexaenoic acid(DHA)/5-fluorouracil(5-FU) on the human gastric cancer cell line AGS and examine the underlying mechanism.METHODS: AGS cells were cultured and treated with... AIM: To explore the synergistic effect of docosahexaenoic acid(DHA)/5-fluorouracil(5-FU) on the human gastric cancer cell line AGS and examine the underlying mechanism.METHODS: AGS cells were cultured and treated with a series of concentrations of DHA and 5-FU alone or in combination for 24 and 48 h. To investigate the synergistic effect of DHA and 5-FU on AGS cells, the inhibition of cell proliferation was determined by MTT assay and cell morphology. Flow cytometric analysis was also used to assess cell cycle distribution, and the expression of mitochondrial electron transfer chain complexes(METCs)?Ⅰ, Ⅱ and Ⅴ in AGS cells was further determined by Western blot analysis. RESULTS: DHA and 5-FU alone or in combination could markedly suppress the proliferation of AGS cells in a significant time and dose-dependent manner. DHA markedly strengthened the antiproliferative effect of 5-FU, decreasing the IC50 by 3.56-2.15-fold in an apparent synergy. The morphological changes of the cells were characterized by shrinkage, cell membrane blebbing and decreased adherence. Cell cycle analysis showed a shift of cells into the G0/G1 phase from the S phase following treatment with DHA or 5-FU(G0/G1 phase: 30.04% ± 1.54% vs 49.05% ± 6.41% and 63.39% ± 6.83%, respectively, P < 0.05; S phase: 56.76% ± 3.14% vs 34.75% ± 2.35% and 25.63% ± 2.21%, respectively, P < 0.05). Combination treatment of DHA and 5-FU resulted in a significantly larger shift toward the G0/G1 phase and subsequent reduction in S phase(G0/G1 phase: 69.06% ± 2.63% vs 49.05% ± 6.41% and 63.39% ± 6.83%, respectively, P < 0.05; S phase: 19.80% ± 4.30% vs 34.75% ± 2.35% and 25.63% ± 2.21%, respectively, P < 0.05). This synergy was also reflected in the significant downregulation of the expression of METCs in AGS cells.CONCLUSION: Synergistic anticancer properties of DHA and 5-FU may involve interference with energy production of AGS cells via downregulation of METCs and cell cycle arrest. 展开更多
关键词 Docosahexaenoic acid Gastric cancer 5-fluorouracil Cell line Mitochondria
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STAT5-c-Myc-axis regulates B cell metabolism in vaccinated individuals and COVID-19 recovered patients 认领 引用
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作者 Lu Yang Linhua Wang +9 位作者 Qian Liu Xu Zhang Yuexin Luo Junbiao Xue Xinpu Yang Maria G.Byazrova Alexander V.Filatov Sheng-Ce Tao Wei Xiao Chaohong Liu 《Virologica Sinica》 SCIE CAS CSCD 2025年第4期571-578,共8页
SARS-CoV-2 infection and vaccination both trigger immune responses. The former leads to naturally acquired immunity, while the latter induces active immunity through artificial means. However, the distinct immune effe... SARS-CoV-2 infection and vaccination both trigger immune responses. The former leads to naturally acquired immunity, while the latter induces active immunity through artificial means. However, the distinct immune effects of vaccination and infection, as well as their underlying mechanisms, require further clarification. In this study, we compared the peripheral B cell differentiation, serological differences and the expression level of BCR signaling molecules between the vaccinated and recovered group. The vaccinated group exhibited reduced RBD-specific B cell differentiation and lower CD86 signal intensity on memory B cells, but enhanced BCR signaling in B cells. Regarding metabolic signaling, the vaccinated group had elevated expression levels of pS6, c-Myc, pmTOR, and pSTAT5, suggesting that the STAT5-c-Myc axis plays a role in regulating B cell metabolism. Additionally, proteome microarray analysis revealed that the serum of the vaccinated group contained higher levels of IgG antibodies against the SARS-CoV-2 N-Nter protein and IgA antibodies specific to the SARS-CoV-2 S1 protein. In summary, these findings indicate that the vaccinated group develops a more robust coronavirus-specific immune response, with enhanced BCR signaling and metabolic activity compared to the recovered group. These insights might contribute to the optimization of SARS-CoV-2 vaccine design. 展开更多
关键词 SARS-CoV-2 B cell Vaccine STAT5 c-Myc
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Impact of miR-214-5p and miR-21-5p from hypoxic endometrial exosomes on human umbilical cord mesen-chymal stem cell function 认领 引用 被引量：1
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作者 Jin-Wei Zhang 《World Journal of Stem Cells》 SCIE 2025年第2期137-140,共4页
Exosomes derived from hypoxic endometrial epithelial cells are pivotal in cellular communication and tissue repair,offering new perspectives on reproductive health.This manuscript highlights the study by Zhang et al,w... Exosomes derived from hypoxic endometrial epithelial cells are pivotal in cellular communication and tissue repair,offering new perspectives on reproductive health.This manuscript highlights the study by Zhang et al,which investigates the effects of miR-214-5p and miR-21-5p in hypoxic cell-derived exosomes on human umbilical cord mesenchymal stem cells.The study reveals that low levels of these microRNAs activate the signal transducer and activator of transcription 3 signaling pathway,enhancing human umbilical cord mesenchymal stem cell migration and differentiation.These findings provide novel insights into therapeutic strategies for improving endometrial health and addressing infertility linked to thin endometrium. 展开更多
关键词 MiR-214-5p MiR-21-5p Hypoxic endometrial epithelial cells Exosomes Human umbilical cord mesenchymal stem cells Signal transducer and activator of transcription 3 signaling Thin endometrium Infertility
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Long non-coding RNA GAS5 promotes PC12 cells differentiation into Tuj1-positive neuron-like cells and induces cell cycle arrest 认领 引用 被引量：6
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作者 He-Yan Zhao Sheng-Tong Zhang +7 位作者 Xiang Cheng Hao-Ming Li Lei Zhang Hui He Jian-Bing Qin Wei-Ye Zhang Yan Sun Guo-Hua Jin 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第12期2118-2125,共8页
Growth arrest-specific 5 (GAS5) is an anti-oncogene that has been extensively studied in tumors. However, research on GAS5 in the context of nervous system disease is rare at present. This study aimed to investigate t... Growth arrest-specific 5 (GAS5) is an anti-oncogene that has been extensively studied in tumors. However, research on GAS5 in the context of nervous system disease is rare at present. This study aimed to investigate the role of the long non-coding RNA GAS5 in rat pheochromocytoma cells (PC12 cells). GAS5-overexpressing lentivirus was transfected into PC12 cells, and expression levels of GAS5 and C-myc were detected by real-time PCR. Ratios of cells in S phase were detected by 5-ethynyl-2′-deoxyuridine. Immunohistochemical staining was used to detect the immunoreactivity of neuron microtubule markers Tuj1, doublecortin, and microtubule-associated protein 2. Apoptosis was detected by flow cytometry, while expression of acetylcholine in cells was detected by western blot assay. We found that GAS5 can promote PC12 cells to differentiate into Tuj1-positive neuron-like cells with longer processes. In addition, cell proliferation and cell cycle were significantly suppressed by GAS5, whereas it had no effect on apoptosis of PC12 cells. Our results indicate that GAS5 could increase the expression of choline acetyltransferase and acetylcholine release. Thus, we speculate that GAS5 is beneficial to the recovery of neurons and the cholinergic nervous system. 展开更多
关键词 nerve regeneration growth arrest-specific 5 PC12 cell neuron proliferation cell cycle choline acetyltransferase acetylcholine Alzheimer's disease neural regeneration
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