Archives of biochemistry and biophysics最新文献_第2页

The lncRNA SENCR of polymorphism rs12420823 drives breast cancer progression and its overexpression regulates this process via the miR-3648/FOXD3 axis 多态性rs12420823的lncRNA SENCR驱动乳腺癌进展，其过表达通过miR-3648/FOXD3轴调控这一过程。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-01-07 DOI: 10.1016/j.abb.2026.110732

Lingjun Kong , Jiajie Xue , Jiaqi Yang , Jianxing Chen , Caiqin Mo

The roles of long noncoding RNA SENCR (lncRNA SENCR) and its variant rs12420823 in triple-negative breast cancer (TNBC) susceptibility, progression, and molecular mechanisms remain unclear. thus, this study investigated the association of lncRNA SENCR and rs12420823 with TNBC risk and prognosis and explored the functional SENCR/miR-3648/FOXD3 axis. This study involving 205 TNBC patients and 203 controls, the rs12420823 polymorphism was genotyped and clinically correlated, revealing that the C allele is associated with reduced TNBC risk, while the TT genotype correlates with larger tumors, lymph node metastasis, advanced stage, and poorer survival. Prognosis was evaluated using Kaplan. The lncRNA SENCR and its variant rs12420823 play significant roles in TNBC Meier survival analysis and multivariate Cox regression. Through qRT-PCR analysis of serum and cell lines, lncRNA SENCR was found downregulated in TNBC, especially in TT genotype carriers. Mechanistic investigations, including luciferase reporter and RNA immunoprecipitation (RIP) assays, demonstrated that lncRNA SENCR directly binds to miR-3648, which targets FOXD3. Functional assays such as MTT and Transwell experiments showed that SENCR overexpression suppresses TNBC cell proliferation, migration, and invasion, effects reversed by a miR-3648 mimic. Furthermore, SENCR upregulates FOXD3 mRNA, an effect also abolished by miR-3648. In conclusion, the rs12420823 C allele confers protection against TNBC, and lncRNA SENCR acts as a tumor suppressor by sponging miR-3648 to regulate FOXD3, underscoring its prognostic and therapeutic relevance.

长链非编码RNA SENCR （lncRNA SENCR）及其变体rs12420823在三阴性乳腺癌（TNBC）易感性、进展和分子机制中的作用尚不清楚。因此，本研究探讨了lncRNA senr和rs12420823与TNBC风险和预后的关系，并探讨了功能的senr /miR-3648/FOXD3轴。本研究纳入205例TNBC患者和203例对照，对rs12420823多态性进行基因分型和临床相关性分析，发现C等位基因与TNBC风险降低相关，而TT基因型与肿瘤较大、淋巴结转移、晚期和较差的生存率相关。采用Kaplan评估预后。lncRNA SENCR及其变体rs12420823在TNBC Meier生存分析和多变量Cox回归中发挥重要作用。通过对血清和细胞系的qRT-PCR分析，发现lncRNA SENCR在TNBC中表达下调，尤其是在TT基因型携带者中。包括荧光素酶报告基因和RNA免疫沉淀（RIP）实验在内的机制研究表明，lncRNA SENCR直接与靶向FOXD3的miR-3648结合。MTT和Transwell实验等功能分析表明，SENCR过表达抑制TNBC细胞的增殖、迁移和侵袭，这种作用被miR-3648模拟物逆转。此外，SENCR上调FOXD3 mRNA，这一作用也被miR-3648所消除。综上所述，rs12420823c等位基因对TNBC具有保护作用，lncRNA SENCR通过抑制miR-3648调控FOXD3而发挥抑癌作用，强调了其预后和治疗相关性。

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引用次数: 0

The regulation of CP-31398 on liquid-liquid phase separation of p53 CP-31398对p53液-液分离的调控作用

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-01-16 DOI: 10.1016/j.abb.2026.110735

Yang Liu , Chang Xu , Fangming Jiang , Xiaorong Yang

The tumor suppressor p53 could regulate the cell cycle arrest, DNA repair and apoptosis. It underwent liquid-liquid phase separation (LLPS) to form droplets. CP-31398 was thought as the activator of p53. In this work, the regulation of CP-31398 on the LLPS of p53 was investigated. The results revealed that CP-31398 promoted the LLPS of p53, delayed the solidification of p53 droplets and increased the mobility of p53 droplets. It also enhanced the tolerance of p53 droplets to the negative charges, and improved the phase behavior of heterotypic p53-pol II CTD droplets. The p53-CP-31398 droplets were driven by hydrogen bonds, hydrophobic and electrostatic interactions. These findings clarified that CP-31398 could elevate the transcriptional function of p53 probably by modulating the phase behavior. The study provided new insights into the regulation mechanism of p53 and potential therapeutic avenues for cancer.

肿瘤抑制因子p53可调控细胞周期阻滞、DNA修复和细胞凋亡。经液液相分离（LLPS）形成液滴。CP-31398被认为是p53的激活剂。本研究探讨了CP-31398对p53 LLPS的调控作用。结果表明，CP-31398促进了p53的LLPS，延缓了p53液滴的凝固，增加了p53液滴的迁移率。增强了p53液滴对负电荷的耐受性，改善了异型p53-pol II CTD液滴的相行为。p53-CP-31398液滴由氢键、疏水和静电相互作用驱动。这些发现表明，CP-31398可能通过调控相行为来提高p53的转录功能。该研究为p53的调控机制和潜在的癌症治疗途径提供了新的见解。

引用次数: 0

RNA binding motif protein 15 promotes intracerebral hemorrhage progression by regulating mitophagy through E2F transcription factor 1 RNA结合基序蛋白15通过E2F转录因子1调控线粒体自噬促进脑出血进展

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-01-20 DOI: 10.1016/j.abb.2026.110746

Jiwei Sun , Ning Li , Yesen Zhang, Jian Song, Yi Han

RNA binding motif protein 15 (RBM15) has been implicated in the progression of various diseases. However, its role in intracerebral hemorrhage (ICH) remains inadequately understood. To investigate RBM15's involvement in ICH, an ICH model was established using HT-22 cells and C57BL/6 mice. Elevated RBM15 expression levels were observed, suggesting its critical role in ICH pathogenesis. Our study further revealed that RBM15 depletion significantly mitigated ICH-induced brain injury and enhanced neurological function. Furthermore, RBM15 was found to mediate the N6-methyladenosine (m6A) methylation of E2F transcription factor 1 (E2F1) mRNA, thereby enhancing its stability. Further analysis confirmed that RBM15 regulates mitophagy via E2F1, with E2F1 overexpression effectively counteracting mitophagy in the absence of RBM15. Collectively, these findings indicate that targeting RBM15 may offer a promising therapeutic strategy for ICH.

RNA结合基序蛋白15 （RBM15）与多种疾病的进展有关。然而，其在脑出血（ICH）中的作用仍不充分了解。为了研究RBM15在脑出血中的作用，我们采用HT-22细胞和C57BL/6小鼠建立脑出血模型。RBM15表达水平升高，提示其在脑出血发病机制中起关键作用。我们的研究进一步表明，RBM15缺失可显著减轻ich诱导的脑损伤并增强神经功能。此外，RBM15被发现介导E2F转录因子1 (E2F1) mRNA的n6 -甲基腺苷（m6A）甲基化，从而增强其稳定性。进一步分析证实，RBM15通过E2F1调控线粒体自噬，在RBM15缺失的情况下，E2F1过表达可有效抵消线粒体自噬。总的来说，这些发现表明靶向RBM15可能为脑出血提供一种有希望的治疗策略。

引用次数: 0

Structural and biochemical characterization of a GH5_22 enzyme from the seaweed-derived thermophile Geobacillus thermodenitrificans OS27 海藻源嗜热反硝化地杆菌OS27中GH5_22酶的结构和生化表征

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-01-16 DOI: 10.1016/j.abb.2026.110736

Wonkyu Lee , Tomoya Hino , Kenta Fujii , Sugue Tanimoto , Reno Naka , Koya Hara , Takaki Okamoto , Fumiyoshi Okazaki , Shingo Nagano , Takashi Ohshiro , Hirokazu Suzuki

Geobacillus thermodenitrificans OS27 is a seaweed-derived thermophile that harbors a GH5_22 gene (bxlA) that encodes for a glycoside hydrolase fused with the cyclin box domain. In this study, we characterized the catalytic activity, enzymatic properties, three-dimensional structure, and physiological role of the gene product, GtBxlA. The enzyme was produced as a thermostable dimer, acting on p-nitrophenyl-β-d-xylopyranoside among 23 substrates. β-1,4-Linked xylooligosaccharides were also hydrolyzed from the nonreducing end. The activity indicated that GtBxlA functions as an exo-β-1,4-xylosidase. We determined the crystal structure of the Glu188Ala variant complexed with β-1,4-xylotriose at 1.52 Å resolution. GtBxlA exhibited an atypical (β/α)₈-barrel architecture. The cyclin box constituted a single α-helix within the core barrel and a lid-like domain that contributes to dimer formation. Structural analysis revealed that Glu188 and Glu318 are positioned to serve as the acid/base and nucleophile catalysts, respectively. Alanine mutagenesis confirmed the essential role of Glu188 and Glu318 in catalysis. We also determined the ligand-free structure of the Glu188Ala variant. Both structures were almost identical; however, a loop at the substrate entry site was fixed in the ligand-free structure, suggesting a conformational change upon substrate binding. Although bxlA deletion did not affect β-1,4-xylan utilization, its expression was induced by β-1,4-xylan. These observations suggest that G. thermodenitrificans OS27 employed GtBxlA in utilizing β-1,4-xylan. Notably, GtBxlA could hydrolyze β-1,3-linked xylooligosaccharides. This highlights the possibility that GtBxlA also assists the host in utilizing β-1,3-xylan, which is abundant in certain seaweeds.

Geobacillus thermodenitrificans OS27是一种源自海藻的嗜热菌，其含有GH5_22基因（bxlA），该基因编码与细胞周期蛋白盒结构域融合的糖苷水解酶。在这项研究中，我们表征了基因产物GtBxlA的催化活性、酶学性质、三维结构和生理作用。该酶是一种耐热二聚体，在23种底物中作用于对硝基苯-β-d-木吡喃苷。β-1,4-连接的低聚木糖也从非还原端水解。活性表明GtBxlA具有外显β-1,4-木糖苷酶的功能。我们在1.52 Å分辨率下确定了Glu188Ala变体与β-1,4-木糖三糖络合的晶体结构。GtBxlA呈现非典型的（β/α）8桶结构。周期蛋白盒在核心筒内由单个α-螺旋和一个有助于二聚体形成的盖子状结构域组成。结构分析表明，Glu188和Glu318分别被定位为酸/碱和亲核催化剂。丙氨酸诱变证实了Glu188和Glu318在催化中的重要作用。我们还确定了Glu188Ala变体的无配体结构。两种结构几乎完全相同；然而，底物进入位点的环固定在无配体结构中，表明底物结合后构象发生了变化。虽然bxlA缺失不影响β-1,4-木聚糖的利用，但它的表达受到β-1,4-木聚糖的诱导。这些结果表明，G. thermodenaficans OS27利用GtBxlA利用β-1,4-木聚糖。值得注意的是，GtBxlA可以水解β-1,3-连接的低聚木糖。这突出了GtBxlA也可能帮助宿主利用β-1,3-木聚糖，β-1,3-木聚糖在某些海藻中丰富。

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引用次数: 0

Systems analysis of the kinetics of in vitro transcription from interactions of T7 RNA polymerase and DNA T7 RNA聚合酶与DNA相互作用的体外转录动力学系统分析。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-01-16 DOI: 10.1016/j.abb.2026.110737

Nathan M. Stover , Marieke De Bock , Julie Chen, Jacob Rosenfeld, Maria del Carme Pons Royo, Allan S. Myerson, Richard D. Braatz

The in vitro transcription reaction (IVT) is of growing importance for the manufacture of RNA vaccines and therapeutics. While the kinetics of the microscopic steps of this reaction (promoter binding, initiation, and elongation) are well studied, the rate law of overall RNA synthesis that emerges from this system is unclear. In this work, we show that a model that incorporates both initiation and elongation steps is essential for describing trends in IVT kinetics in conditions relevant to RNA manufacturing. In contrast to previous reports, we find that the IVT reaction can be either initiation- or elongation-limited depending on solution conditions. This initiation-elongation model is also essential for describing the effect of salts, which disrupt polymerase-promoter binding, on transcription rates. Polymerase-polymerase interactions during elongation are incorporated into our modeling framework and found to have nonzero but unidentifiable effects on macroscopic transcription rates. Finally, we develop an extension of our modeling approach to quantitatively describe and experimentally evaluate RNA- and DNA-templated mechanisms for the formation of double-stranded RNA (dsRNA) impurities.

体外转录反应（IVT）在RNA疫苗和治疗药物的生产中越来越重要。虽然该反应的微观步骤（启动子结合、起始和延伸）的动力学已经得到了很好的研究，但从该系统中产生的整个RNA合成的速率规律尚不清楚。在这项工作中，我们证明了一个包含起始和延伸步骤的模型对于描述与RNA制造相关条件下IVT动力学的趋势是必不可少的。与以前的报道相反，我们发现IVT反应可以是引发或延伸限制取决于溶液条件。这种起始-延伸模型对于描述破坏聚合酶启动子结合的盐对转录率的影响也是必不可少的。延伸期间的聚合酶-聚合酶相互作用被纳入我们的建模框架，并发现对宏观转录率有非零但无法识别的影响。最后，我们开发了我们的建模方法的扩展，以定量描述和实验评估RNA和dna模板形成双链RNA （dsRNA）杂质的机制。

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引用次数: 0

The B-box domain and the PRY-SPRY domain of recombinant human MG53 are critical for its inhibitory effects on angiogenesis 重组人MG53的B-box结构域和PRY-SPRY结构域是其抑制血管生成的关键。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-02-03 DOI: 10.1016/j.abb.2026.110757

Qin Yu , Jiarui Hu , Shuangshuang Yuan , Tian Li , Yongjie Li , Xin Deng , Ni Chen , Mao Luo , Jianbo Wu , Liqun Wang

Our previous studies identified recombinant human MG53 (rhMG53) as a novel regulator that inhibits endothelial cell migration and angiogenesis by modulating focal adhesion kinase (FAK) signaling. However, the specific structural component of rhMG53 responsible for its inhibitory effects on angiogenesis has not yet been elucidated. Here, we generated a series of rhMG53 mutants and found that both the ΔB mutant (deletion of the B-box domain of rhMG53) and the ΔS mutant (deletion of the PRY-SPRY domain of rhMG53) failed to decrease endothelial migration and tube formation in vitro, indicating the critical roles of these two domains in rhMG53-regulated angiogenesis. Mechanistically, only the ΔB mutant failed to interact with FAK, suggesting that the B-box domain may function as a FAK-interacting domain. Notably, both the B-box and PRY-SPRY domains are essential for the inhibitory effects of rhMG53 on the activation of the FAK/Src/paxillin signaling pathway. Furthermore, the significance of these two domains in the anti-angiogenic activity of rhMG53 was further confirmed in the aortic ring vessel outgrowth assay and in the alkaline-induced corneal neovascularization model. These findings highlight the novel roles of the B-box and PRY-SPRY domains in rhMG53-regulated angiogenesis and enhance our understanding of rhMG53 in modulating endothelial functions.

我们之前的研究发现重组人MG53 （rhMG53）是一种通过调节局灶黏着激酶（FAK）信号抑制内皮细胞迁移和血管生成的新型调节剂。然而，rhMG53抑制血管生成作用的具体结构成分尚未被阐明。在这里，我们生成了一系列rhMG53突变体，发现ΔB突变体（删除rhMG53的B-box结构域）和ΔS突变体（删除rhMG53的PRY-SPRY结构域）在体外都不能减少内皮迁移和管的形成，这表明这两个结构域在rhMG53调控的血管生成中起着关键作用。从机制上讲，只有ΔB突变体不能与FAK相互作用，这表明B-box结构域可能是与FAK相互作用的结构域。值得注意的是，B-box和PRY-SPRY结构域对于rhMG53对FAK/Src/paxillin信号通路激活的抑制作用至关重要。此外，这两个结构域在rhMG53抗血管生成活性中的意义在主动脉环血管生长试验和碱诱导的角膜新生血管模型中得到进一步证实。这些发现强调了B-box和PRY-SPRY结构域在rhMG53调节血管生成中的新作用，并增强了我们对rhMG53调节内皮功能的理解。

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引用次数: 0

Platelet-rich plasma enhances anti-apoptotic and paracrine effects of bone marrow mesenchymal stem cells through the PI3K/Akt pathway 富血小板血浆通过PI3K/Akt通路增强骨髓间充质干细胞的抗凋亡和旁分泌作用。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-01-30 DOI: 10.1016/j.abb.2026.110754

Zhiyao Zhao, Hairui Zhang, Fangzheng Zhou, Yaohui Yang, Bingzhe Huang, Xiaoning Liu

Previous studies have shown that bone marrow aspirate concentrate (BMAC) can promote tendon-bone interface healing in a rabbit chronic rotator cuff tear model, but its underlying mechanism of action has not been fully elucidated. We suspected that the synergistic effect of platelet-rich plasma (PRP) and bone marrow mesenchymal stem cells (BMSCs) in BMAC might improve the anti-apoptotic and paracrine effects of BMSCs. Here, we prepared rabbit PRP and BMSCs, and found that PRP not only attenuated hypoxic and serum-free medium (H/SF)-induced apoptosis of BMSCs but also increased the protein expression of Bcl2, which was reduced by H/SF, and decreased the protein expression of cleaved caspase 9, and cleaved caspase 3, which was elevated by H/SF, in BMSCs. PRP also promoted the expression of growth factors (PDGF, VEGF, TGF-β1, and IGF-1) in BMSCs. In a chronic rotator cuff tear rabbit model, the PRP + BMSC-treated group showed higher values of biomechanical properties than the BMSC-treated group. Furthermore, results also showed that PRP promoted the phosphorylation of Akt in BMSCs, and inhibition of the PI3K/Akt pathway not only increased the apoptosis of BMSCs cultured with PRP, but it also decreased the concentration of growth factors in culture medium of BMSCs. Collectively, our results indicate that PRP enhances the anti-apoptotic and paracrine effects of BMSCs, and this might be related to the activation of the PI3K/Akt pathway in BMSCs by PRP.

既往研究表明骨髓浓缩物（bone marrow aspirate concentrate， BMAC）能促进兔慢性肩袖撕裂模型的肌腱-骨界面愈合，但其作用机制尚未完全阐明。我们推测富血小板血浆（PRP）和骨髓间充质干细胞（BMSCs）在BMAC中的协同作用可能会提高BMSCs的抗凋亡和旁分泌作用。我们制备了兔PRP和骨髓间充质干细胞，发现PRP不仅能减弱缺氧和无血清培养基（H/SF）诱导的骨髓间充质干细胞凋亡，还能增加被H/SF降低的Bcl2蛋白表达，降低被H/SF升高的cleaved caspase 9和cleaved caspase 3蛋白表达。PRP还能促进骨髓间充质干细胞中生长因子（PDGF、VEGF、TGF-β1、IGF-1）的表达。在兔慢性肩袖撕裂模型中，PRP + bmscs处理组比bmscs处理组表现出更高的生物力学性能。此外，结果还表明，PRP促进了骨髓间充质干细胞中Akt的磷酸化，抑制PI3K/Akt通路不仅增加了PRP培养的骨髓间充质干细胞的凋亡，还降低了骨髓间充质干细胞培养基中生长因子的浓度。综上所述，我们的研究结果表明，PRP增强了骨髓间充质干细胞的抗凋亡和旁分泌作用，这可能与PRP激活骨髓间充质干细胞中的PI3K/Akt通路有关。

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引用次数: 0

The SNCA-AS1/miR-138-5p/HIF1A Axis: Implications for diagnosis and cellular pathogenesis in acute cerebral infarction SNCA-AS1/miR-138-5p/HIF1A轴：急性脑梗死的诊断和细胞发病机制的意义

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2025-12-15 DOI: 10.1016/j.abb.2025.110705

Pingting Chen , Yilin Feng , Cu Bai

Background

Acute cerebral infarction (ACI) is a common cerebrovascular disease with complex pathogenesis. The role of non-coding RNAs in ACI warrants further investigation. To investigate the expression, diagnostic value, and molecular mechanism of SNCA-AS1 in ACI.

Methods

Blood samples from 125 ACI patients and matched controls were collected. RT-qPCR detected SNCA-AS1, miR-138-5p, and HIF1A expression. ROC curves assessed diagnostic value. BV-2 cells were cultured under oxygen-glucose deprivation (OGD) conditions, with RT-qPCR used to measure molecular expression. Dual-luciferase assays and RNA immunoprecipitation (RIP) were employed to verify the intermolecular interactions within the axis. ELISA determined cytokine levels, CCK-8 and Transwell assays evaluated proliferation and migration, and flow cytometry detected apoptosis. Data were statistically analyzed using t-tests, ANOVA, and correlation analysis.

Results

SNCA-AS1 and HIF1A were upregulated, while miR-138-5p was downregulated in ACI patients. SNCA-AS1 showed a diagnostic AUC of 0.849. Experiments confirmed SNCA-AS1 binds miR-138-5p and regulates HIF1A. SNCA-AS1 or HIF1A knockdown alleviated inflammation, suppressed proliferation and migration, and promoted apoptosis, effects reversed by miR-138-5p inhibitor.

Conclusion

SNCA-AS1 participates in ACI pathogenesis through the miR-138-5p/HIF1A axis and may serve as a potential diagnostic marker.

背景：急性脑梗死（Acute cerebral infarction， ACI）是一种常见的脑血管疾病，发病机制复杂。非编码rna在ACI中的作用有待进一步研究。探讨SNCA-AS1在ACI中的表达、诊断价值及分子机制。方法：采集125例急性脑损伤患者及对照组的血液标本。RT-qPCR检测SNCA-AS1、miR-138-5p和HIF1A的表达。ROC曲线评估诊断价值。在氧葡萄糖剥夺（OGD）条件下培养BV-2细胞，采用RT-qPCR检测分子表达。采用双荧光素酶测定和RNA免疫沉淀（RIP）来验证轴内的分子间相互作用。ELISA检测细胞因子水平，CCK-8和Transwell检测细胞增殖和迁移，流式细胞术检测细胞凋亡。数据采用t检验、方差分析和相关分析进行统计学分析。结果：在ACI患者中SNCA-AS1和HIF1A表达上调，miR-138-5p表达下调。SNCA-AS1的诊断AUC为0.849。实验证实SNCA-AS1结合miR-138-5p并调控HIF1A。SNCA-AS1或HIF1A敲低可减轻炎症，抑制增殖和迁移，促进细胞凋亡，miR-138-5p抑制剂逆转了这一作用。结论：SNCA-AS1通过miR-138-5p/HIF1A轴参与ACI发病，可能作为潜在的诊断标志物。

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引用次数: 0

ADMSC-derived exosomes promote diabetic wound healing by inhibiting neutrophil extracellular traps formation through delivering miR-92a-1-5p admsc衍生的外泌体通过递送miR-92a-1-5p抑制中性粒细胞胞外陷阱形成，从而促进糖尿病伤口愈合。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-01-31 DOI: 10.1016/j.abb.2026.110755

Wei Li , Hong Zhang , Pengxing Bai , Hui Wang , Feng Hou , Zheqi Zhou , Wenbo Li

Adipose-derived mesenchymal stem cell-derived exosomes (ADMSC-ex) have demonstrated remarkable efficacy in promoting diabetic wound healing. However, the underlying mechanisms remain largely elusive. In this study, we showed the healing process of skin wounds in diabetic rats was notably delayed, but this delay was mitigated by the administration of ADMSCs-ex. Neutrophil extracellular traps (NETs) formation was significantly upregulated in the skin wounds from the diabetes group. ADMSCs-ex administration attenuated this upregulation. The upregulation of S100A9 was confirmed in wound tissues from diabetic rats, as well as neutrophils induced by high glucose. ADMSCs-ex administration significantly reduced S100A9 protein expression via delivering miR-92a-1-5p in vitro. In vivo study showed that miR-92a-1-5p knockdown obstructed the promotional effect of ADMSCs-ex on diabetic wound healing and NETs formation. In conclusion, this study provides evidence that ADMSCs-ex accelerate diabetic wounds healing via a conserved miR-92a-1-5p/S100A9 pathway. These findings suggest that these exosomes loaded with miR-92a-1-5p may represent a promising therapeutic approach for the management of impaired healing of diabetic wounds.

脂肪源性间充质干细胞源性外泌体（ADMSC-ex）在促进糖尿病伤口愈合方面表现出显著的功效。然而，潜在的机制在很大程度上仍然难以捉摸。在本研究中，我们发现糖尿病大鼠皮肤伤口的愈合过程明显延迟，但ADMSCs-ex可以缓解这种延迟。中性粒细胞胞外陷阱（NETs）的形成在糖尿病组皮肤伤口中显著上调。ADMSCs-ex可减弱这种上调。S100A9在糖尿病大鼠创面组织及高糖诱导的中性粒细胞中表达上调。ADMSCs-ex通过体外递送miR-92a-1-5p显著降低S100A9蛋白表达。体内研究表明，miR-92a-1-5p敲低阻断了ADMSCs-ex对糖尿病创面愈合和NETs形成的促进作用。总之，本研究提供了ADMSCs-ex通过保守的miR-92a-1-5p/S100A9途径加速糖尿病伤口愈合的证据。这些发现表明，这些装载miR-92a-1-5p的外泌体可能代表了一种有希望的治疗糖尿病伤口愈合受损的方法。

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引用次数: 0

Synthesis, characterization, antimicrobial and antibiofilm potential of novel bimetallic selenium/zinc oxide nanoparticles: Kinetic study and membrane leakage reaction mechanism determination 新型双金属硒/氧化锌纳米颗粒的合成、表征、抗菌和抗生物膜电位：动力学研究和膜渗漏反应机理测定

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-04-01 Epub Date: 2026-01-29 DOI: 10.1016/j.abb.2026.110749

Mohamed A.M. Ali , Alyaa S. Abdel Halim , Ahmed I. El-Batal , Gharieb S. El-Sayyad

Antibiotic-resistant biofilms present significant challenges to healthcare, emphasizing the need for unique antimicrobial nanomaterials. This study developed bimetallic selenium/zinc oxide (Se/ZnO) nanoparticles (NPs) through environmentally friendly co-precipitation to improve structural stability, optical characteristics, antimicrobial efficacy, and antibiofilm activity. The ZnO, Se, and Se/ZnO NPs have been examined using X-ray diffraction, DLS, EDX elemental analysis, zeta potential, scanning electron microscopy, EDX-mapping, and diffuse reflectance spectroscopy (DRS). Se NPs, ZnO NPs, and Se/ZnO NPs have crystallite sizes of 12.13, 40.88, and 51.14 nm, respectively. Se/ZnO NPs' antibacterial potential had been checked, the minimum quantity required to stop microbial growth was performed, and their capacity to inhibit the formation of biofilms was evaluated to determine how effectively they can combat bacteria that cause wound infections and single-celled yeast organisms. The membrane leakage assay was used to conduct kinetic analysis and determine the potential mechanism of the antimicrobial reaction. Promising antimicrobial activity has been demonstrated by the produced Se/ZnO NPs for the tested bacteria and unicellular fungi. Staphylococcus aureus (with a zone of inhibition (ZOI) of 28.33 mm), Escherichia coli, Candida albicans (19.0 mm ZOI), Klebsiella pneumoniae, and 19 mm surrounding Candida tropicalis, 18.33 mm around Staphylococcus epidermidis, and 17.33 mm near Enterobacter calcoaceticus were among the bacteria it demonstrated a strong antimicrobial activity. All examined bacteria in the integrated samples had minimum inhibitory concentrations (MIC) from 15.62 to 62.5 μg/mL. A promising MIC of 7.812 μg/mL was shown by Se/ZnO NPs against C. albicans. The favorable conclusions indicated that the developed nano-formula may be used to fight dangerous microbes in the biomedical areas in the future to overcome their resistance.

耐抗生素生物膜对医疗保健提出了重大挑战，强调需要独特的抗菌纳米材料。本研究通过环境友好共沉淀法制备了双金属硒/氧化锌（Se/ZnO）纳米粒子（NPs），以提高其结构稳定性、光学特性、抗菌功效和抗生物膜活性。采用x射线衍射、DLS、EDX元素分析、zeta电位、扫描电子显微镜、EDX作图和漫反射光谱（DRS）对ZnO、Se和Se/ZnO NPs进行了表征。Se NPs、ZnO NPs和Se/ZnO NPs的晶粒尺寸分别为12.13、40.88和51.14 nm。研究人员检查了Se/ZnO NPs的抗菌潜力，进行了阻止微生物生长所需的最小量，并评估了它们抑制生物膜形成的能力，以确定它们对抗引起伤口感染的细菌和单细胞酵母生物的有效程度。采用膜渗漏法进行动力学分析，确定抗菌反应的可能机制。制备的Se/ZnO NPs对细菌和单细胞真菌具有良好的抑菌活性。金黄色葡萄球菌（抑制区为28.33 mm）、大肠杆菌、白色念珠菌（抑制区为19.0 mm）、肺炎克雷伯菌和热带念珠菌周围19 mm、表皮葡萄球菌周围18.33 mm、钙酸肠杆菌周围17.33 mm均表现出较强的抑菌活性。综合样品中所有细菌的最低抑菌浓度（MIC）为15.62 ~ 62.5 μg/mL。Se/ZnO NPs抗白色念珠菌的MIC值为7.812 μg/mL。研究结果表明，该纳米配方可用于生物医学领域对抗危险微生物，克服其耐药性。

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