BACKGROUND:The pathological progression of ischemic stroke (IS) is closely associated with oxidative stress and neuronal apoptosis, yet current therapeutic strategies remain substantially limited. The critical role of the transcriptional coactivator TAZ in this process, particularly in modulating oxidative damage, is not well defined. METHODS:By integrating a middle cerebral artery occlusion (MCAO) mouse model with an oxygen-glucose deprivation/reoxygenation (OGD/R) neuronal injury model, this study reveals the critical role of the transcriptional coactivator TAZ in modulating oxidative damage via Foxo1 and by coordinating with the deubiquitination activity of ubiquitin-specific protease 1 (Usp1). RESULTS:Single-cell RNA sequencing combined with transcriptomic datasets demonstrated spatiotemporal dynamics of TAZ expression in ischemic brain tissues, showing significant downregulation at 24 h post-reperfusion. This decline inversely correlated with peaks of oxidative stress markers (glutathione peroxidase [GSH-px], superoxide dismutase [SOD]) and pro-inflammatory cytokines (interleukin-6 [IL-6], interleukin-1β [IL-1β]). Enhanced TAZ expression reduced cerebral infarct volume, improved cerebral blood flow, and ameliorated neurological and cognitive deficits. Mechanistically, TAZ promoted Foxo1 transcriptional activity, upregulating antioxidant genes SOD2 and catalase, thereby suppressing reactive oxygen species (ROS) accumulation and neuronal apoptosis. CONCLUSIONS:Usp1 counteracted TAZ ubiquitination to stabilize its protein levels, synergistically reinforcing Foxo1 DNA-binding capacity. The coordinated action of Usp1 and TAZ attenuated oxidative stress, neuronal death, and infarct progression. These findings establish the Usp1-TAZ-Foxo1 axis as a critical regulator of antioxidant defense and neuronal survival, providing a theoretical foundation for targeted therapeutic strategies in IS.

BACKGROUND:Albumin-binding prodrugs represent a pharmacological strategy to improve systemic stability and tumor exposure of cytotoxic agents. Legumain, an asparagine endopeptidase selectively activated in the acidic tumor microenvironment, provides a mechanism for tumor-specific prodrug activation. In this study, we developed WC10-003, a legumain-responsive albumin-binding prodrug of belotecan, and investigated its pharmacological properties and antitumor activity in ovarian cancer models. METHODS:WC10-003 was synthesized by conjugating belotecan to a legumain-cleavable peptide linker. Albumin association, plasma stability, and enzymatic activation were evaluated to characterize its pharmacological behavior. Antitumor efficacy was assessed in ovarian cancer xenograft models and compared with irinotecan and belotecan. Transcriptomic analysis was performed to explore treatment-associated signaling alterations, and immunohistochemistry and flow cytometry were used to evaluate changes in tumor-associated macrophage polarization. RESULTS:Following intravenous administration, WC10-003 rapidly associated with endogenous albumin, forming a stable circulating complex that prolonged systemic exposure and enhanced tumor drug accumulation. In ovarian cancer xenograft models, WC10-003 produced significantly greater tumor growth inhibition than irinotecan or belotecan, consistent with improved pharmacokinetic and tumor exposure profiles. Transcriptomic profiling revealed suppression of PI3K-AKT-related signaling pathways associated with tumor growth. In addition, immunophenotypic analyses demonstrated a shift in tumor-associated macrophages toward a less immunosuppressive phenotype. Combination treatment with WC10-003 and anti-PD-1 antibody further enhanced antitumor efficacy, suggesting that pharmacologically optimized prodrug activation can sensitize tumors to immune checkpoint blockade. CONCLUSION:WC10-003 exhibits favorable pharmacological properties, including albumin-mediated stabilization and legumain-dependent tumor activation, resulting in enhanced antitumor efficacy in preclinical ovarian cancer models. These findings highlight a pharmacologically driven prodrug strategy for improving cytotoxic drug performance and support its further evaluation in combination with immunotherapy.

Sepsis-associated encephalopathy (SAE) is a common and serious complication of sepsis, characterized by neuroinflammation and cognitive dysfunction, yet its molecular mechanisms remain unclear. This study aimed to investigate the role of heat shock protein 90α (HSP90α) in microglial NLRP3 inflammasome activation and cognitive impairment in SAE, and to explore the therapeutic potential of a small molecule compound, nicotinamide N-oxide (NAMO). SAE models were established using cecal ligation and puncture (CLP) in mice and LPS/ATP stimulated primary microglial cells/BV-2 cells. A combination of H&E/Nissl/TUNEL staining, transcriptomics, immunoblotting, qPCR, immunofluorescence, ELISA, mtDNA release, co-immunoprecipitation, molecular docking, AAV stereotaxic delivery, and pharmacological/siRNA interventions were utilized. Results showed that HSP90α expression was significantly upregulated in microglia during SAE. HSP90α facilitated NLRP3 inflammasome activation and exacerbated cognitive dysfunction in SAE by inducing mitochondrial dysfunction and promoting the release of mitochondrial DNA (mtDNA). Mechanistically, HSP90α interacted with PPP3CA, which facilitated Drp1 dephosphorylation at Ser637, triggering mitochondrial fragmentation and mtDNA release. Importantly, we identified that NAMO binds directly to HSP90α, inhibits the HSP90α-PPP3CA-Drp1 axis, reduces mtDNA release, and suppresses NLRP3 inflammasome activation. Administration of NAMO significantly alleviated cognitive impairment in SAE mice. Collectively, our findings reveal a novel HSP90α-PPP3CA-Drp1-mtDNA-NLRP3 signaling pathway in microglial activation and cognitive injury during SAE, and propose NAMO as a promising therapeutic candidate for SAE intervention.

Environmental residues of the fungicide difenoconazole (DFZ) have been shown to pose a threat to mammals. However, the risk assessment of DFZ for cultured carp remains unclear. The aim of this study was to investigate the adverse effects of DFZ on carp liver and their molecular mechanisms by simulating the environmental contamination concentrations of DFZ. Our results showed that DFZ induced structural damage in the liver, including edema, vacuolation, and congestion. In addition, DFZ residues were detected in liver tissues. Mechanistically, DFZ causes mitochondrial dysfunction by promoting Ca2+ transfer from the endoplasmic reticulum (ER) to mitochondria via IP3R, leading to the onset of ROS burst and apoptosis, and the inhibition of Nrf2 antioxidant function by DFZ also results in uncontrolled ROS. Mitophagy was also activated intracellularly to counteract mitochondrial damage. Interestingly, treatment with 2-APB alleviated mitochondrial dysfunction, restored the mitochondrial membrane potential, and inhibited apoptosis by blocking the translocation of Ca2+ from the ER to the mitochondria. Metabolomic analysis revealed that DFZ disrupted energy metabolism in carp liver, whereas 2-APB reversed DFZ-induced metabolic alterations. In conclusion, the present study elucidates the threat of DFZ to carp liver and highlights the mechanism of damage, thereby helping to explain the impact of agriculture on the aquatic environment.

PURPOSE:The aim of this study is to delve into the value of N6-Methyladenosine (m6A)-associated genes (MAGs) in pancreatic cancer (PC) prognosis. METHODS:PC sequencing data and corresponding clinicopathological information were retrieved from GEO and TCGA databases. We filtered 19 MAGs in PC specimens and implemented functional annotation in biology. Later, the m6A modification pattern was stratified into m6Acluster A-B according to MAG expression levels, and further categorized into genecluster A-C based on differentially expressed genes between m6Acluster A and B. Next, a MAG-based prognostic prediction model was established by the least absolute shrinkage and selection operator (LASSO) regression analysis and multivariate Cox regression analysis. At last, the role of KRT7 in PC were explored. RESULTS:We found m6Acluster A pattern presented enrichment pathways associated with cell apoptosis, proliferation, migration, and cancer pathways. Additionally, high-risk group displayed more dismal prognosis and a higher programmed death-ligand 1 expression. The survival prediction ability of the model was verified in three independent PC GEO datasets. KRT7 is the most momentous risk gene in the established prognostic model. Among 18 clinical samples, the KRT7 protein in the surviving patient samples is lower than that in the deceased patient samples. We also identified elevated expression of KRT7 in PC tumor tissues compared to normal tissues using GEPIA 2. Then, the metastasis of PC cells was promoted by overexpressed KRT7 in vitro and in vivo. And IGF2BP3 upregulated KRT7 by increasing the mRNA stability of KRT7. CONCLUSIONS:The PPM built based on CXCL5, LY6K and KRT7 is an encouraging biomarker to define the prognosis. Additionally, IGF2BP3 promoted KRT7 by stabilizing mRNA of KRT7. And KRT7 promoted the metastasis of PC cells by promoting EMT.

Arsenic trioxide (ATO) has exhibited remarkable efficacy in treating acute promyelocytic leukemia (APL), primarily through promoting the degradation of the PML-RARα fusion protein. However, ATO alone fails to confer any survival benefit to non-APL acute myeloid leukemia (AML) patients and exhibits limited efficacy when used in combination with other agents. Here, we explored the general toxicity mechanisms of ATO in APL and potential drugs that could be combined with ATO to exhibit synergistic lethal effects on other AML. We demonstrated that PML-RARα degradation and ROS upregulation were insufficient to cause APL cell death. Based on the protein synthesis of different AML cells and their sensitivity to ATO, we established a correlation between ATO-induced cell death and protein synthesis. Our findings indicated that ATO induced cell death by damaging nascent polypeptides and causing ribosome stalling, accompanied by the activation of the ZAKα-JNK pathway. Furthermore, ATO-induced stress activated the GCN2-ATF4 pathway, and ribosome-associated quality control cleared damaged proteins with the assistance of p97. Importantly, our data revealed that inhibiting p97 enhanced the effectiveness of ATO in killing AML cells. These explorations paved the way for identifying optimal synthetic lethal drugs to enhance ATO treatment on non-APL AML.

目的:探讨PBL教学方法在血管外科临床实习中的应用价值.方法:选取2017年3 月至2019年3 月我院血管外科临床专业本科及硕士研究生共60 名,按随机数字表法分为试验组和对照组,每组各30 人.对照组采取传统的LBL教学方法,试验组采取采取PBL教学方法.比较两组学生教学之后的基础理论知识、病例分析成绩及两组学生的教学效果.结果:考核后,试验组学生基础理论知识成绩高于对照组,但差异不具有统计学意义(P>0.05);试验组学生病例分析成绩高于对照组,差异具有统计学意义(P<0.05).考核后,试验组学生在文献检索能力、学习兴趣、对疾病的认识、手术操作、总体满意度、团队协作能力和探索创新能力方面的评分显著高于对照组,差异具有统计学意义(P<0.05).两组学生在语言表达能力和综合分析能力方面的评分比较,差异不具有统计学意义(P>0.05).结论:PBL教学方法在血管外科临床实习中的应用效果显著,值得推广.

Abstract Our study aims to explore whether transplantation of exogenous NSCs could be an effective means to deal with neuronal death. In this study, horseradish peroxidase (HRP) nerve tracing and rat olfactory bulb injury model were established; olfactory function was evaluated; HRP nerve tracing assay was conducted; primary NSCs was prepared, identified, differentiated into astrocytes, and used for treatment SD rats with injured olfactory bulb. Results showed that the foraging time was longer in the disconnected olfactory bulb group than the undisconnected group; HRP nerve tracing showed negative TMB staining in the disconnected olfactory bulb injury site and positive TMB staining in the corresponding undisconnected olfactory bulb site, which confirmed the successful establishment of the rat olfactory bulb disconnected injury model. The primary rat cortical-derived NSCs were confirmed positive by Nestin immunofluorescence staining, and then transplanted to the olfactory nerve of olfactory bulb disconnected rats after Brdu labeling. The foraging time in the NSCs transplanted group was shorter than that in the untransplanted group, and the transplanted NSCs migrated from the olfactory nerve to the site of olfactory bulb injury, showing positive cells for Nestin and Brdu staining in the olfactory bulb anterior nucleus, and a large number of positive cells for GFAP staining in the lateral edge of the olfactory ventricle (olfactory bulb inner sublayer and granular layer, etc.). In this study, we found that transplanted exogenous NSCs exerted a migratory repair effect on olfactory bulb dissociation injury in rats, providing a reference for clinical treatment of olfactory nerve injury.

目的 探究血管内成型治疗在高龄急性缺血性脑卒中(acute ischemic stroke,AIS)患者中的应用效果.方法 收集2019年1月 ～2021年1月于连云港市第一人民医院收治的因AIS行机械取栓联合血管成型治疗患者的临床资料,随访患者术后6个月mRS评分.以70岁为界限,定义年龄≥70岁为高龄组,年龄<70岁为低龄组.结果 212例AIS患者中行血管内成型治疗的患者42例,其中高龄组患者9例,平均年龄为76.1±3.7岁,发生颅内出血转化1例(11.1％),预后良好3例(33.3％);低龄组患者33例,平均年龄为60.5±9.1岁,发生出血转化11例(33.3％),预后良好10例(30.3％).两组患者在出血转化及预后不良的发生率比较,差异无统计学意义(P>0.05).结论 高龄AIS患者机械取栓联合血管内成型治疗,并不增加患者症状性颅内出血及不良预后的发生率.

AML ranks second in the most common types of leukemia diagnosed in both adults and children. Necroptosis is a programmed inflammatory cell death form reported to be an innate immune effector against microbial and viral pathogens and recently has been found to play an eventful role in the oncogenesis, progression, and metastasis of cancer. This study is designed to explore the potential value of necroptosis in predicting prognostic and optimizing the current therapeutic strategies for AML patients. We collected transcriptome and clinical data from the Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) databases and selected necroptosis-related genes with both differential significance and prognostic value. Six genes (YBX3, ZBP1, CDC37, ALK, BRAF, and BNIP3) were incorporated to generate a risk model with the implementation of multivariate Cox regression. The signature was proven to be an independent prognostic predictor in both training and validation cohorts with hazard ratios (HRs) of 1.51 (95% CI: 1.33–1.72) and 1.57 (95% CI: 1.16–2.12), respectively. Moreover, receiver operating characteristic (ROC) curve was utilized to quantify the predictive performance of the signature and satisfying results were shown with the area under the curve (AUC) up to 0.801 (3-year) and 0.619 (3-year), respectively. In addition, the subtyping of AML patients based on the risk signature demonstrated a significant correlation with the immune cell infiltration and response to immunotherapy. Finally, we incorporated risk signature with the classical clinical features to establish a nomogram which may contribute to the improvement of clinical management. To conclude, this study identified a necroptosis-related signature as a novel biomarker to improve the risk stratification, to inform the immunotherapy efficacy, and to indicate the therapeutic option of targeted therapy.

前瞻性分析蚌埠医学院第一附属医院收治的108例非血栓性髂静脉压迫综合征患者的多平面静脉造影资料，测量其下腔静脉（IVC）直径、左髂总静脉（LCIV）开口0、20、40、60、80 mm处髂静脉直径、IVC与LCIV所成角度、LCIV长度。最终解除压迫后LCIV直径为（15.6±1.9）mm，髂外静脉（LEIV）为（11.2±1.8）mm，IVC为（19.6±3.2）mm，LCIV长度为（61.3±11.0）mm，IVC与LCIV夹角为36.4°±15.8°。本研究显示下腔静脉与髂总静脉、髂外静脉变化存在一致性；髂总静脉长度与髂外静脉直径、下腔静脉与髂静脉所成角度呈负相关。

Objective:To identify the influencing factors of pathological progression in patients with Budd-Chiari syndrome (BCS) after endovascular treatment.Methods:Clinical data of 55 patients with BCS admitted the First Affiliated Hospital of Bengbu Medical College from January 2014 to December 2020 were retrospectively analyzed. Among them, 24 patients were male and 31 female, aged (48±11) years on average. The informed consents of all patients were obtained and the local ethical committee approval was received. After the first endovascular treatment, 31 patients were diagnosed with simple diaphragm type BCS, 18 cases with short-segment lesion type BCS and 6 cases with long-segment lesion type BCS. All enrolled patients received multiple endovascular treatments for consecutive 3 years or longer. The pathological progression of lesion was observed. The effects on the changes of lesions by age upon first admission, sex, frequency of surgeries, average patency time, type of lesion upon first admission and duration of taking anticoagulants were evaluated by multivariate Logistic regression analysis.Results:55 patients received 288 times of endovascular treatment which was balloon dilatation. The success rate of surgery was 100%. The vascular recanalization rate was 100%. The median time of the first patency was 9 months, 8 months for the second patency, 8 months for the third patency and 8 months for the last patency. During the treating period, the lesion type changed in 22 patients. Among them, simple diaphragm type progressed to short-segment lesion type in 13 cases, short-segment lesion type evolved to long-segment lesion type in 5, short-segment lesion type complicated with thrombosis in 3, and long-segment lesion type progressed to mixed lesion type in 1. Multivariate Logistic regression analysis demonstrated that the time of use of anticoagulants was an independent factor affecting the progression of BCS (OR=0.124, 95%CI: 0.032-0.479, P=0.002).Conclusions:Patients with BCS have the tendency of progression after endovascular treatment. Thrombosis is a critical factor for disease progression. Regular use of anticoagulants might retard the progression of lesions.

Oncogene-induced tumorigenesis results in the variation of epigenetic modifications, and in addition to promoting cell immortalization, cancer cells undergo more intense cellular stress than normal cells and depend on other support genes for survival. Chromosomal translocations of mixed-lineage leukemia (MLL) induce aggressive leukemias with an inferior prognosis. Unfortunately, most MLL-rearranged (MLL-r) leukemias are resistant to conventional chemotherapies. Here, we showed that hydroxyurea (HU) could kill MLL-r acute myeloid leukemia (AML) cells through the necroptosis process. HU target these cells by matrix metallopeptidase 2 (MMP2) deficiency rather than subordinate ribonucleotide reductase regulatory subunit M2 (RRM2) inhibition, where MLL directly regulates MMP2 expression and is decreased in most MLL-r AMLs. Moreover, iron chelation of HU is also indispensable for inducing cell stress, and MMP2 is the support factor to protect cells from death. Our preliminary study indicates that MMP2 might play a role in the nonsense-mediated mRNA decay pathway that prevents activation of unfolding protein response under innocuous endoplasmic reticulum stress. Hence, these results reveal a possible strategy of HU application in MLL-r AML treatment and shed new light upon HU repurposing.

ABSTRACT Osteosarcoma is characterized by diverse genetic mutations, including single-nucleotide variants (SNVs), which can complicate clinical outcomes of the treatment. This study identified key mutations or polymorphisms in genes that correlate with osteosarcoma prognoses. A total of 110 patients with osteosarcoma were assigned to “good” or “poor” cohorts depending on their 5-year disease-free survival (DFS) after surgery and chemotherapeutic treatment. We performed next-generation sequencing analysis of tumor tissues for prognosis-associated SNVs in 315 tumorigenesis-related genes, followed by modeling of clinical outcomes for these patients using random forest classification via a support vector machine (SVM). Data from the Chinese Millionome Database were used to compare SNV frequency in osteosarcoma patients and healthy people. SVM screening identified 17 nonsynonymous SNVs located in 15 genes, of which rs17224367 and rs3733406 (located in MSH2 and FAT1, respectively) were strongly correlated with osteosarcoma prognosis. These results were verified in a 26-patient validation cohort, confirming that these SNVs could be used to predict prognosis. These results demonstrated that two SNVs located in MSH2 and FAT1 are associated with prognosis of osteosarcoma patients. © 2022 American Society for Bone and Mineral Research (ASBMR).

目的 探讨血清同型半胱氨酸(homocysteine,Hcy)及不同血脂成分对高血压脑出血的影响.方法 收集笔者医院2018年1月 ～2019年12月确诊原发性高血压患者的病例资料1248例,以高血压脑出血为研究组(n=339),原发性高血压为对照组(n=909).收集性别、年龄、入院血压值、血脂及血清Hcy水平.计数数据采用 χ2检验,计量数据采用t检验.结果 研究组共纳入339例患者,对照组909例,研究组患者血清Hcy、胆固醇(cholesterol,TC)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)水平显著高于对照组,差异均有统计学意义(P均<0.05).Logistic回归分析显示,高同型半胱氨酸血症(HHcy)(OR=6.97,95％CI:3.29～14.80,P=0.01)、TC(OR=1.13,95％CI:1.19～1.50,P=0.01)、LDL-C(OR=5.78,95％CI:3.49～9.59,P=0.01)及年龄(OR=1.05,95％CI:1.03～1.06,P=0.01)是高血压患者发生脑出血的危险因素.ROC曲线结果显示,Hcy、TC、LDL-C及三者联合预测高血压脑出血的AUC面积分别为0.697、0.862、0.833和0.869.结论 高血压脑出血患者拥有更高的血清Hcy、TC、LDL-C水平,且3项指标联合对高血压脑出血的诊断具有较高的预测能力.

目的 探究急性缺血性脑卒中(acute ischemic stroke,AIS)患者经支架联合负压抽吸(Solumbra)技术取栓后发生责任血管区颅内出血转化(hemorrhagic transformation,HT)的危险因素.方法 收集2019年1月 ～2021年6月于徐州医科大学附属连云港医院采用Solumbra技术治疗的212例AIS患者的临床资料,其中颅内出血转化组50例,未出血组162例,比较两组患者临床资料的差异.计量资料分析采用t检验,计数资料分析采用 χ2检验,并检验危险因素对取栓术后颅内出血的诊断价值.结果 出血转化组发病年龄、发病至介入取栓时间、手术总时间、支架取栓操作次数均高于未出血组,差异均有统计学意义(P均<0.05).多因素Logistic回归分析显示,年龄(OR=1.075,95％CI:1.034～1.117,P=0.001)、取栓次数(OR=1.877,95％CI:1.309～2.692,P=0.001)是AIS患者Solumbra技术取栓后发生颅内出血转化的危险因素.受试者工作特征曲线结果显示,年龄、支架取栓次数及二者联合预测术后颅内出血的曲线下面积分别是0.70、0.69、0.85,其敏感度分别为68.0％、50.0％、86.0％,特异性分别为65.0％、86.0％、70.6％,年龄、取栓次数的截断值分别是67.5岁、2.5次.Spearman相关分析显示,患者的责任血管位置、低白蛋白血症及高糖化血红蛋白水平与入院高NIHSS评分显著相关(P<0.05).结论 高龄AIS患者Solumbra技术下多次取栓可能增加术后颅内出血转化的风险.

Osteosarcoma (OS) is a primary malignant bone neoplasm with high frequencies of tumor metastasis and recurrence. Although the Akt/PKB signaling pathway is known to play key roles in tumorigenesis, the roles of cyclin-dependent kinase-like 3 (CDKL3) in OS progression remain largely elusive. We have demonstrated the high expression levels of CDKL3 in OS human specimens and comprehensively investigated the role of CDKL3 in promoting OS progression both in vitro and in vivo. We found that CDKL3 regulates Akt activation and its downstream effects, including cell growth and autophagy. The up-regulation of CDKL3 in OS specimens appeared to be associated with Akt activation and shorter overall patient survival (P = 0.003). Our findings identify CDKL3 as a critical regulator that stimulates OS progression by enhancing Akt activation. CDKL3 represents both a biomarker for OS prognosis, and a potential therapeutic target in precision medicine by targeting CDKL3 to treat Akt hyper-activated OS.

脑卒中为威胁人民生命健康的首要因素,出血性脑卒中是其重要的类型.脑出血作为出血性脑卒中的常见类型,是高血压严重并发症之一.同型半胱氨酸及血脂是除高血压、糖尿病、抽烟、饮酒等传统危险因素外,引起脑出血的新型危险因素,但同型半胱氨酸及血脂对脑出血的影响机制尚未完全明确,本研究对高血压脑出血病人与同型半胱氨酸及血脂的相关性研究作一综述.

Objective:To compare drug-coated balloon (DCB) and standard angioplasty balloon (SAB) in the treatment of postoperative in-stent restenosis (ISR) in patients with arteriosclerosis obliterans (ASO) of the lower extremity.Methods:From Jan 2017 to Dec 2018, 43 ISR patients after percutaneous transluminal angioplasty for ASO of the lower extremity at our hospital were enrolled.Patients were divided into 2 groups with 18 patients treated by DCB and 25 by SAB. The patients were followed up for 6~12 months.Results:There was no significant difference in the incidence of complications between DCB group and SAB group ( P>0.05).Compared with that in SAB group, the plasma level of ET-1 in DCB group was lower while NO was higher at 6, 24 h and 2 weeks after surgery ( P<0.05), there was no significant difference in P-selectin ( P>0.05). The ABI values in both groups increased, and that in DCB group were higher than SAB group at 6 and 12 months after surgery ( P<0.05). The lumen loss in DCB group at 6 and 12 months after surgery was significantly lower ( P<0.05). At 6 and 12 months, the primary patency of target lesions in the DCB group was 100.00% and 88.89%, which was higher than the 72.00% and 52.00% in the SAB group ( P<0.05); the CD-TLR rate in the DCB group was 11.11%, which was lower than 48.00% in the SAB group ( P<0.05). Conclusion:DCB comes with lower postoperative ISR in ASO patients of the lower extremity.