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Paeoniflorin Attenuates Fumonisin B1-Induced Cytotoxicity by Inhibiting the p38 MAPK Pathway in 3D4/21 Cells 芍药苷通过抑制p38 MAPK通路降低伏马菌素b1诱导的3D4/21细胞的细胞毒性
4区 生物学 Q4 BIOLOGY Pub Date : 2025-11-26 DOI: 10.1134/s1062359025602319
Sun Li, Jianbo Yang, Jian Jin
Fumonisin B1 (FB1), a water-soluble mycotoxin produced by Fusarium moniliforme, poses significant health risks to both humans and animals through widespread contamination of agricultural commodities. Paeoniflorin (PF), a bioactive monoterpene glycoside extracted from Paeonia lactiflora, exhibits potent anti-inflammatory and antioxidant properties. This study investigated the protective effects of PF against FB1-induced cytotoxicity in porcine alveolar macrophages (3D4/21) and explored the underlying molecular mechanisms. Cells were treated with FB1 (50 μg/mL) in combination with PF (100 μg/mL) for 24 h. Results demonstrated that PF significantly attenuated FB1-induced cytotoxicity by improving cell viability, restoring cytoskeletal and tight junction protein expression (α-Tubulin and ZO-1), and reducing apoptosis and oxidative stress. PF treatment successfully restored the balance of inflammatory cytokines (including IL-6, IL-8, IL-1β, IFN-α, and INF-γ) that had been dysregulated in 3D4/21 cells upon FB1 exposure. Transcriptomic analysis revealed that PF reversed FB1-induced gene expression alterations, particularly within clusters associated with cellular stress responses. Further investigation identified the p38 MAPK pathway as a critical mechanism through which PF exerts its protective effects, with significant downregulation of key pathway components including MAPK14, MAP2K3, ATF2, and MAPKAPK2 in cells co-treated with PF and FB1. These findings provide mechanistic insights into the protective effects of PF against environmental mycotoxins and suggest its potential application in mitigating FB1-induced agricultural and ecological toxicity.
伏马菌素B1 (FB1)是由念珠镰刀菌产生的一种水溶性真菌毒素,通过对农产品的广泛污染,对人类和动物构成重大健康风险。芍药苷(Paeoniflorin, PF)是一种从芍药中提取的具有生物活性的单萜苷,具有抗炎和抗氧化的作用。本研究探讨了PF对fb1诱导的猪肺泡巨噬细胞毒性的保护作用(3D4/21),并探讨了其潜在的分子机制。FB1 (50 μg/mL)联合PF (100 μg/mL)作用细胞24 h,结果表明,PF通过提高细胞活力,恢复细胞骨架蛋白和紧密连接蛋白(α-微管蛋白和ZO-1)表达,减少细胞凋亡和氧化应激,显著减弱FB1诱导的细胞毒性。PF治疗成功恢复了FB1暴露后3D4/21细胞中失调的炎症细胞因子(包括IL-6、IL-8、IL-1β、IFN-α和INF-γ)的平衡。转录组学分析显示,PF逆转了fb1诱导的基因表达改变,特别是在与细胞应激反应相关的簇内。进一步的研究发现p38 MAPK通路是PF发挥其保护作用的关键机制,在PF和FB1共处理的细胞中,关键通路成分包括MAPK14、MAP2K3、ATF2和MAPKAPK2显著下调。这些发现为PF对环境真菌毒素的保护作用提供了机制见解,并表明其在减轻fb1诱导的农业和生态毒性方面的潜在应用。
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引用次数: 0
Optimization of RAPD-PCR Assay for Assessing Genetic Variability in Brachyuran Crab Populations from Freshwater Ecosystems 淡水生态系统短爪蟹种群遗传变异RAPD-PCR评价方法的优化
4区 生物学 Q4 BIOLOGY Pub Date : 2025-09-04 DOI: 10.1134/s1062359024610139
Menakshi Dhar, Seema Langer
Genetic analysis of any species depends upon the yield of DNA samples. In the present study, randomly amplified polymorphic DNA (RAPD-PCR) was optimized for the crab species inhabiting the freshwater ecosystems. In the initial step, the optimal concentration of PCR components and cycling conditions were standardized by altering the parameters of PCR reaction such as PCR buffer, magnesium chloride, dNTPs, primer, Taq polymerase, template DNA, denaturation time, annealing temperature and time, and volume of the reaction. Results indicated that the RAPD-PCR optimization system was 2 µL of 10X PCR buffer with 1.5 mM MgCl2, 2 µL of 2.5 mM dNTPs, 4 µL of primer (10 picomoles/µL), 0.25 µL of 5U Taq polymerase, 1 µL of template DNA (50 ng/µL) and nuclease-free water to make the total volume of 20 µL with denaturation time of 1 min at 94°C and an annealing temperature of 35°C. The optimized PCR and its programming conditions were then used to study the genetic diversity within the populations of freshwater crab, found in the different locations of the Jammu region. Assessment of genetic diversity among any species or the population of the species is essential for aquaculture practices.
任何物种的遗传分析都取决于DNA样本的产量。本研究利用随机扩增多态性DNA (RAPD-PCR)技术对生活在淡水生态系统中的蟹类进行了优化。在初始步骤中,通过改变PCR反应的参数,如PCR缓冲液、氯化镁、dNTPs、引物、Taq聚合酶、模板DNA、变性时间、退火温度和时间、反应体积等,标准化PCR组分的最佳浓度和循环条件。结果表明,RAPD-PCR优化体系为:10X PCR缓冲液2µL,含1.5 mM MgCl2, 2.5 mM dNTPs 2µL,引物4µL(10皮摩尔/µL), 5U Taq聚合酶0.25µL,模板DNA 1µL (50 ng/µL),无核酸酶水,使总体积为20µL,变性时间为1 min, 94℃,退火温度为35℃。利用优化后的PCR及其编程条件,对查谟地区不同地点淡水蟹种群的遗传多样性进行了研究。对任何物种或该物种种群的遗传多样性进行评估对水产养殖实践至关重要。
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引用次数: 0
Two New Records of Boletoid Mushrooms (Boletaceae) from India 标题印度甜菇科甜菇类两新记录
4区 生物学 Q4 BIOLOGY Pub Date : 2025-08-01 DOI: 10.1134/s1062359024613533
S. Rajput, S. Singh, Kanad Das, Yash Pal Sharma
During an extensive and regular survey conducted in the less-explored coniferous forests of Jammu, India, some interesting specimens of boletoid mushrooms were collected. Thorough morphological characterisation followed by two-gene molecular phylogenetic analyses of two specimens, revealed two interesting species: Rubroboletus himalayensis and Phylloporus nigrisquamus, representing first report from India. Their detailed descriptions, illustrations, phylogenetic inferences, and comprehensive comparisons with corresponding similar taxa are also discussed.
在对印度查谟较少开发的针叶林进行的广泛而定期的调查中,收集了一些有趣的boletoid蘑菇标本。对两个标本进行形态学分析和双基因分子系统发育分析,发现了两个有趣的物种:喜马拉雅红毛猴(Rubroboletus喜马拉雅山)和黑毛猴(Phylloporus nigrisquamus),这是印度的首次报道。本文还讨论了它们的详细描述、图解、系统发育推断以及与相应相似分类群的综合比较。
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引用次数: 0
Clonal Integration between Zoysia Ramets Improves Overall Resistance under Heterogeneous Pb and/or Pyrene Stresses by Modulating AsA-GSH Cycle 结缕草品种间克隆整合通过调节AsA-GSH循环提高对非均质Pb和/或芘胁迫的整体抗性
4区 生物学 Q4 BIOLOGY Pub Date : 2025-08-01 DOI: 10.1134/s1062359024610942
Yichen Liu, Sunan Xu, Xuemei Li, Lihong Zhang
Pb and Pyrene, prevalent in soil, significantly affect plants. Ascorbate-glutathione (AsA-GSH) cycle is crucial for plant antioxidant defense mechanisms. Understanding the clonal integration of clonal plants in heterogeneous contaminated soil is important. This work investigates the potential effects of clonal integration on the key players in specifically the metabolism, AsA-GSH cycle, in Zoysia japonica ramets under three heterogeneous stresses (Pb and/or Pyrene) and two stolon connection statuses (connected and disconnected ramets). The results showed that connected stressed ramets exhibit higher biomass accumulation and lower H2O2 content compared to disconnected stressed ramets. This can be attributed to the enhancement of Ascorbate Peroxidase (APX) enzyme activity, the preservation of Glutathione Reductase (GR), Dehydroascorbate Reductase (DHAR), and Monodehydroascorbate Reductase (MDHAR) activity. Furthermore, there was a reduction in the decline of Ascorbic Acid (AsA) and Glutathione (GSH), and a decrease in the rise of Dehydroascorbic Acid (DHA) and Glutathione Disulfide (GSSG). Among three heterogeneous stresses, clonal integration performs better under Pb or Pyrene stress than under Pb + Pyrene stress. Our study highlights the vital role of clonal integration in maintaining redox balance and supporting the success of clonal plants in toxic environments, even under severe combined stress.
土壤中普遍存在的铅和芘对植物有显著影响。抗坏血酸-谷胱甘肽(AsA-GSH)循环对植物抗氧化防御机制至关重要。了解异质性污染土壤中无性系植物的克隆整合具有重要意义。本研究研究了在三种不同胁迫(Pb和/或芘)和两种匍匐茎连接状态(连接和断开)下,结缕草株系克隆整合对代谢关键因子AsA-GSH循环的潜在影响。结果表明:连接的应力框架比连接的应力框架具有更高的生物量积累和更低的H2O2含量。这可归因于抗坏血酸过氧化物酶(APX)酶活性的增强,谷胱甘肽还原酶(GR),脱氢抗坏血酸还原酶(DHAR)和单脱氢抗坏血酸还原酶(MDHAR)活性的保存。此外,抗坏血酸(AsA)和谷胱甘肽(GSH)的下降幅度减小,脱氢抗坏血酸(DHA)和谷胱甘肽二硫(GSSG)的上升幅度减小。在3种非均质胁迫下,Pb或芘胁迫下克隆整合的效果优于Pb +芘胁迫。我们的研究强调了无性系整合在维持氧化还原平衡和支持无性系植物在有毒环境中成功的重要作用,即使是在严重的综合胁迫下。
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引用次数: 0
Gene Ontology and Identification of Transcription Factors Related to Key Genes Involved in Drought Stress Tolerance of Soybean (Glycine max L.) 大豆(Glycine max L.)抗旱关键基因的基因本体及相关转录因子鉴定
4区 生物学 Q4 BIOLOGY Pub Date : 2025-07-26 DOI: 10.1134/s1062359024612679
Mostafa Alamholo, Aladdin Sheikhmous Murad
Transcription factors (TFs) are a group of proteins that regulate drought stress-responsive genes by binding to DNA at specific elements in promoter regions. No combinatorial analysis has been performed to identify the TFs and gene ontology (GO) involved in drought stress tolerance so far. Soybean microarray datasets were analyzed through R language packages. To identify TFs, sequences of down and up-regulated genes involved in drought stress tolerance using multiple promoter analysis was used. Common GO down and up-regulated genes were identified by Venny v2.1. Up-regulated key TFs were associated with AT-Hook, homeodomain, MYb/SANT, TBP, and WRKY and down-regulated key TFs related to Dof, bHLH, bZIP, and ZF-HD. Biological processes (BP) of up-regulated genes mainly belonged to fatty acid and photosynthesis processes and down-regulated genes mostly related to response to abiotic stresses. Molecular function (MF) of up-regulated genes mainly related to transferase enzymes and down-regulated genes mostly connected to regulators and inhibitory enzymes. Based on the results of this study, it is possible to understand the molecular mechanisms related to drought stress in soybean, and key TFs can be used to control the expression of genes related to drought stress in plant breeding and genetic engineering.
转录因子(Transcription factors, TFs)是一组通过与启动子区域特定元件的DNA结合来调节干旱胁迫应答基因的蛋白质。到目前为止,还没有进行组合分析来确定参与干旱胁迫耐受性的tf和基因本体(GO)。通过R语言包对大豆微阵列数据集进行分析。为了鉴定TFs,利用多启动子分析,对参与干旱胁迫耐受的下调和上调基因序列进行了分析。通过Venny v2.1鉴定常见的GO下调和上调基因。上调的关键tf与AT-Hook、homeodomain、MYb/SANT、TBP和WRKY相关,下调的关键tf与Dof、bHLH、bZIP和ZF-HD相关。上调基因的生物过程(BP)主要属于脂肪酸和光合作用过程,下调基因主要与应对非生物胁迫有关。上调基因的分子功能(MF)主要与转移酶相关,下调基因的分子功能(MF)主要与调节酶和抑制酶相关。基于本研究结果,可以了解大豆干旱胁迫相关的分子机制,并可在植物育种和基因工程中利用关键tf来控制干旱胁迫相关基因的表达。
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引用次数: 0
Tumor-Derived Exosome miR-4661-5p Exerts Tumor-Promoting Effects in Hepatocellular Carcinoma by Targeting ESR1 肿瘤来源的外泌体miR-4661-5p通过靶向ESR1在肝细胞癌中发挥促瘤作用
4区 生物学 Q4 BIOLOGY Pub Date : 2025-06-01 DOI: 10.1134/s1062359024612230
Sha Li, Qian Wang, Lixiu Xu, Mengmeng Liu, Yanni Ma, Wensheng Liu
In the serum exosomes of hepatocellular carcinoma (HCC) patients, miR-4661-5p is reported at a high level. This study aimed to investigate the effect of exosomal miR-4661-5p on the malignant progression of HCC and its mechanism of action. Exosomes were separated from SNU387 cells and identified and miR-4661-5p expression were tested using qRT-PCR. CCK-8, clone formation, and Transwell assays tested the biological characteristics of HCC cells, and flow cytometry determined apoptosis rate. Dual-luciferase reporter gene tests verified the targeting connection between miR-4661-5p and Estrogen receptor alpha (ESR1). Moreover, a subcutaneous graft tumor model was constructed in nude mice. MiR-4661-5p exhibited an elevated level in HCC cells and their exosomes; ESR1 exhibited a notably diminished level in HCC cells; miR-4661-5p targeted and negatively regulated ESR1. After co-culturing with exosomes, Hep3B and Huh7 cells showed heightened levels of miR-4661-5p. Exosomal miR-4661-5p promoted the migration and invasion of HCC cells and depressed apoptosis. Overexpression ESR1 partially declined the promoting impact of over-expressed exosomal miR-4661-5p on the proliferation and invasion ability of Hep3B and Huh7 cells and the suppression of apoptosis. In addition, exosomal or over-expressed miR-4661-5p accelerated tumor expansion in nude mice by regulating the level of ESR1. In conclusion, exosomal miR-4661-5p targets and downregulates ESR1, leading to the promotion of HCC malignant progression, identified exosomal miR-4661-5p and ESR1 as potential therapeutic targets for HCC.
在肝细胞癌(HCC)患者的血清外泌体中,miR-4661-5p被报道处于高水平。本研究旨在探讨外泌体miR-4661-5p对HCC恶性进展的影响及其作用机制。从SNU387细胞中分离外泌体并进行鉴定,并使用qRT-PCR检测miR-4661-5p的表达。CCK-8、克隆形成和Transwell检测HCC细胞的生物学特性,流式细胞术检测细胞凋亡率。双荧光素酶报告基因测试证实了miR-4661-5p与雌激素受体α (ESR1)之间的靶向联系。建立裸鼠皮下移植瘤模型。MiR-4661-5p在HCC细胞及其外泌体中表达水平升高;ESR1在HCC细胞中的表达水平明显降低;miR-4661-5p靶向并负调控ESR1。与外泌体共培养后,Hep3B和Huh7细胞显示miR-4661-5p水平升高。外泌体miR-4661-5p促进HCC细胞的迁移和侵袭,抑制细胞凋亡。过表达ESR1部分减弱了过表达外泌体miR-4661-5p对Hep3B和Huh7细胞增殖和侵袭能力的促进作用以及对凋亡的抑制作用。此外,外泌体或过表达的miR-4661-5p通过调节ESR1的水平加速了裸鼠的肿瘤扩张。总之,外泌体miR-4661-5p靶向并下调ESR1,导致HCC恶性进展,确定外泌体miR-4661-5p和ESR1是HCC的潜在治疗靶点。
{"title":"Tumor-Derived Exosome miR-4661-5p Exerts Tumor-Promoting Effects in Hepatocellular Carcinoma by Targeting ESR1","authors":"Sha Li, Qian Wang, Lixiu Xu, Mengmeng Liu, Yanni Ma, Wensheng Liu","doi":"10.1134/s1062359024612230","DOIUrl":"https://doi.org/10.1134/s1062359024612230","url":null,"abstract":"In the serum exosomes of hepatocellular carcinoma (HCC) patients, miR-4661-5p is reported at a high level. This study aimed to investigate the effect of exosomal miR-4661-5p on the malignant progression of HCC and its mechanism of action. Exosomes were separated from SNU387 cells and identified and miR-4661-5p expression were tested using qRT-PCR. CCK-8, clone formation, and Transwell assays tested the biological characteristics of HCC cells, and flow cytometry determined apoptosis rate. Dual-luciferase reporter gene tests verified the targeting connection between miR-4661-5p and Estrogen receptor alpha (ESR1). Moreover, a subcutaneous graft tumor model was constructed in nude mice. MiR-4661-5p exhibited an elevated level in HCC cells and their exosomes; ESR1 exhibited a notably diminished level in HCC cells; miR-4661-5p targeted and negatively regulated ESR1. After co-culturing with exosomes, Hep3B and Huh7 cells showed heightened levels of miR-4661-5p. Exosomal miR-4661-5p promoted the migration and invasion of HCC cells and depressed apoptosis. Overexpression ESR1 partially declined the promoting impact of over-expressed exosomal miR-4661-5p on the proliferation and invasion ability of Hep3B and Huh7 cells and the suppression of apoptosis. In addition, exosomal or over-expressed miR-4661-5p accelerated tumor expansion in nude mice by regulating the level of ESR1. In conclusion, exosomal miR-4661-5p targets and downregulates ESR1, leading to the promotion of HCC malignant progression, identified exosomal miR-4661-5p and ESR1 as potential therapeutic targets for HCC.","PeriodicalId":55366,"journal":{"name":"Biology Bulletin","volume":"52 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147922076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Armillaria mellea Mycelium Aqueous Extract-Induced Apoptosis in A549 Cells via a Caspase-Mediated Pathway 蜜环菌菌丝水提取物通过caspase介导的途径诱导A549细胞凋亡
4区 生物学 Q4 BIOLOGY Pub Date : 2025-06-01 DOI: 10.1134/s1062359024612436
Junrong Zhang, Chong Zhao
Armillaria mellea is a valuable medicinal and edible fungus widely used in China for its health-promoting properties. It exhibits a broad spectrum of pharmacological activities. Extracts from Armillaria mellea have demonstrated cytotoxic effects against a variety of cancer cell lines. These extracts induce apoptosis and inhibit cell proliferation through multiple mechanisms, including the modulation of critical signaling pathways involved in cell survival and programmed cell death. An additional notable advantage of Armillaria mellea is its non-toxicity, particularly in comparison to conventional chemotherapeutic agents, which frequently lead to adverse side effects. The present study aimed to investigate the anti-lung cancer effects of Armillaria mellea mycelium aqueous (AMMA) extract in the A549 cell line. MTT assay, Hoechst 33342, Fluo-4-AM staining, DCFH-DA staining and ELISA were utilized to evaluate changes in cell viability, nuclear apoptosis, Ca2+ concentration, intracellular reactive oxygen species (ROS) concentration, lactate dehydrogenase (LDH), malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and the protein expression levels of Caspase-3/-8/-9. The results demonstrated that AMMA effectively reduced the survival rate of A549 cells, promoted nuclear apoptosis, calcium ion, intracellular ROS level, LDH and MDA content, inhibited high levels of CAT and SOD, and activated the Caspase-3/-8/-9 apoptosis pathway, ultimately mediating the death of cancer cells. This study confirmed that AMMA has an effective anti-lung cancer activity via the Caspase-3/-8/-9 pathway. These data also clarify the potential of AMMA as a natural product based therapeutic agent for the treatment of non-small cell lung cancer.
蜜环菌(Armillaria mellea)是一种有药用价值的食用菌,具有促进健康的特性,在中国被广泛使用。它具有广泛的药理活性。蜜环菌提取物对多种癌细胞具有细胞毒性作用。这些提取物通过多种机制诱导细胞凋亡和抑制细胞增殖,包括调节参与细胞存活和程序性细胞死亡的关键信号通路。蜜环菌的另一个显著优势是它的无毒性,特别是与经常导致不良副作用的传统化疗药物相比。本研究旨在探讨蜜环菌菌丝水提物(AMMA)对A549细胞株的抗肺癌作用。采用MTT法、Hoechst 33342法、Fluo-4-AM染色法、DCFH-DA染色法和ELISA法检测细胞活力、细胞核凋亡、Ca2+浓度、细胞内活性氧(ROS)浓度、乳酸脱氢酶(LDH)、丙二醛(MDA)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)以及Caspase-3/-8/-9蛋白表达水平的变化。结果表明,AMMA可有效降低A549细胞的存活率,促进细胞核凋亡、钙离子、细胞内ROS水平、LDH和MDA含量,抑制高水平的CAT和SOD,激活Caspase-3/-8/-9凋亡通路,最终介导癌细胞死亡。本研究证实AMMA通过Caspase-3/-8/-9途径具有有效的抗肺癌活性。这些数据也阐明了AMMA作为一种基于天然产物的治疗药物治疗非小细胞肺癌的潜力。
{"title":"Armillaria mellea Mycelium Aqueous Extract-Induced Apoptosis in A549 Cells via a Caspase-Mediated Pathway","authors":"Junrong Zhang, Chong Zhao","doi":"10.1134/s1062359024612436","DOIUrl":"https://doi.org/10.1134/s1062359024612436","url":null,"abstract":"Armillaria mellea is a valuable medicinal and edible fungus widely used in China for its health-promoting properties. It exhibits a broad spectrum of pharmacological activities. Extracts from Armillaria mellea have demonstrated cytotoxic effects against a variety of cancer cell lines. These extracts induce apoptosis and inhibit cell proliferation through multiple mechanisms, including the modulation of critical signaling pathways involved in cell survival and programmed cell death. An additional notable advantage of Armillaria mellea is its non-toxicity, particularly in comparison to conventional chemotherapeutic agents, which frequently lead to adverse side effects. The present study aimed to investigate the anti-lung cancer effects of Armillaria mellea mycelium aqueous (AMMA) extract in the A549 cell line. MTT assay, Hoechst 33342, Fluo-4-AM staining, DCFH-DA staining and ELISA were utilized to evaluate changes in cell viability, nuclear apoptosis, Ca2+ concentration, intracellular reactive oxygen species (ROS) concentration, lactate dehydrogenase (LDH), malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and the protein expression levels of Caspase-3/-8/-9. The results demonstrated that AMMA effectively reduced the survival rate of A549 cells, promoted nuclear apoptosis, calcium ion, intracellular ROS level, LDH and MDA content, inhibited high levels of CAT and SOD, and activated the Caspase-3/-8/-9 apoptosis pathway, ultimately mediating the death of cancer cells. This study confirmed that AMMA has an effective anti-lung cancer activity via the Caspase-3/-8/-9 pathway. These data also clarify the potential of AMMA as a natural product based therapeutic agent for the treatment of non-small cell lung cancer.","PeriodicalId":55366,"journal":{"name":"Biology Bulletin","volume":"52 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147913386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Extracellular Vesicles Derived from Human Umbilical Cord Blood Plasma Protect H2O2-Induced Oxidative Damage by Inhibiting Mitophagy in H9C2 Cells 人脐带血血浆细胞外囊泡通过抑制H9C2细胞自噬来保护h2o2诱导的氧化损伤
4区 生物学 Q4 BIOLOGY Pub Date : 2025-06-01 DOI: 10.1134/s1062359024613132
Yi Jiang, Haoyang Zhou, Rong Cheng, Yanan Pu, Di Wang, Yangyang Jiao, Xinyu Li, Yan Chen
Cardiovascular diseases (CVDs) threaten the human health. Lots of researches suggest that ROS accumulates in cardiomyocytes in CVDs. Excessive mitochondrial autophagy caused by reactive oxygen species (ROS) impairs the function of cardiomyocytes. Here, we found that extracellular vesicles derived human umbilical cord blood plasma (UCB-EV) inhibited oxidative stress-induced mitophagy to promote cell survival. The viability of UCB-EV pre-protected H9C2 cardiomyocytes was maintained after H2O2 exposure. In addition, UCB-EV partially restored mitochondrial membrane potential and promoted mitochondrial biogenesis. Furthermore, PTEN-induced putative kinase 1 (PINK1), a mitochondrial serine/threonine protein kinase, was inhibited by UCB-EV during oxidative stress. We further demonstrate the role of UCB-EV in inhibiting mitophagy to make H9C2 cells survival by PINK1/Parkin pathway. Our findings elucidate the protective mechanism of UCB-EV against oxidative stress in H9C2 cells. These findings reveal the potential role of UCB-EV in alleviate oxidative stress in cardiomyocytes.
心血管疾病威胁着人类的健康。大量研究表明,在心血管疾病中,ROS在心肌细胞中积累。活性氧(ROS)引起的线粒体过度自噬损害心肌细胞的功能。在这里,我们发现细胞外囊泡来源的人脐带血血浆(UCB-EV)抑制氧化应激诱导的线粒体自噬,促进细胞存活。H2O2暴露后,UCB-EV预保护的H9C2心肌细胞的活力得以维持。此外,UCB-EV部分恢复线粒体膜电位,促进线粒体生物发生。此外,pten诱导的推测激酶1 (PINK1),一种线粒体丝氨酸/苏氨酸蛋白激酶,在氧化应激过程中被UCB-EV抑制。我们进一步证明了UCB-EV通过PINK1/Parkin途径抑制有丝分裂使H9C2细胞存活。我们的研究结果阐明了UCB-EV对H9C2细胞氧化应激的保护机制。这些发现揭示了UCB-EV在缓解心肌细胞氧化应激中的潜在作用。
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引用次数: 0
Knockdown of LINC00852 Impairs the In Vitro Activities of Multiple Non-Small Cell Lung Cancer Cells through Activating Cell Autophagy 敲低LINC00852通过激活细胞自噬损害多种非小细胞肺癌细胞的体外活性
4区 生物学 Q4 BIOLOGY Pub Date : 2025-06-01 DOI: 10.1134/s1062359024609753
Boxiong Wu, Haozhe Cheng, Xinran Li, Wenjing Zhang, Qiancheng Li, Shuai Hao
Non-small cell lung cancer (NSCLC) is one of the most lethal types of malignancies around the world. Previously, LINC00852 is a tumor-associated lncRNA which has been verified to participate in affecting the activity of NSCLC cells in our work. However, its underlying molecular mechanism still remains poorly documented. The aim of this work is to further explore the involved regulatory mechanism of LINC00852 on NSCLC cells. Three NSCLC cell lines including H1299, A549 and LTEP-a2 cells were selected. LINC00852 was knockdown through its specific silence molecular ASO. Cell autophagy was analyzed by transmission electron microscope observation, fluorescent adenovirus infection and Western blot assays, respectively. Cell activity was measured through proliferation and colony formation assays. Knockdown the expression of LINC00852 leads to the activation of cell autophagy in three NSCLC cells. Previously, LINC00852 has been proved to act as a ceRNA of miR-29a-3p which further targets LAMTOR1. In this work, miR-29a-3p overexpression or LAMTOR1 knockdown both significantly increased the number of autolysosomes and promoted autophagy flux in NSCLC cells. Strikingly, the proliferation and colony formation abilities of NSCLC cells could be inhibited after treatment of rapamycin, an autophagy activator of cells. The results have indicated that knockdown of LINC00852 could impair the activities of NSCLC cells by activating cell autophagy via the LINC00852/miR-29a-3p/LAMTOR1 axis, which provides scientific guidance for the regulatory mechanism of long non-coding RNA LINC00852 in NSCLC cells, and also lay a theoretical basis for the potential treatment approach of NSCLC.
非小细胞肺癌(NSCLC)是世界上最致命的恶性肿瘤之一。LINC00852是一种肿瘤相关的lncRNA,在我们的工作中已被证实参与影响NSCLC细胞的活性。然而,其潜在的分子机制仍然缺乏文献记载。本研究旨在进一步探讨LINC00852对NSCLC细胞的相关调控机制。选择H1299、A549和ltp -a2三种非小细胞肺癌细胞系。LINC00852通过其特异性沉默分子ASO被敲低。分别用透射电镜观察、荧光腺病毒感染和免疫印迹法分析细胞自噬情况。通过增殖和集落形成试验测定细胞活性。敲低LINC00852的表达可激活三种非小细胞肺癌细胞的自噬。先前,LINC00852已被证明作为miR-29a-3p的ceRNA,进一步靶向LAMTOR1。在本研究中,miR-29a-3p过表达或LAMTOR1敲低均可显著增加NSCLC细胞中自噬酶体的数量并促进自噬通量。引人注目的是,在使用细胞自噬激活剂雷帕霉素后,NSCLC细胞的增殖和集落形成能力可以被抑制。结果表明,敲低LINC00852可通过LINC00852/miR-29a-3p/LAMTOR1轴激活细胞自噬,从而损害NSCLC细胞活性,为长链非编码RNA LINC00852在NSCLC细胞中的调控机制提供了科学指导,也为潜在的NSCLC治疗途径奠定了理论基础。
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引用次数: 0
Schwann Cell Secreted Cyr61 Promotes Motor Neuron Growth 雪旺细胞分泌Cyr61促进运动神经元生长
4区 生物学 Q4 BIOLOGY Pub Date : 2025-06-01 DOI: 10.1134/s1062359024610243
Jing Xu, Yong Ji, Lei Xian, Yawen Zhang, Mengru Ming, Han Wu, Zhang Qi, Mi Shen
Schwann cells (SCs) play a crucial role in the repair of peripheral nerves. This is due to their ability to proliferate, migrate, and provide trophic support to axon regrowth. During peripheral nerve injury, SCs de-differentiate and reprogram to gain the ability to repair nerves. Cysteine-rich 61 (Cyr61/CCN1) is a member of the CCN family of matrix cell proteins, and we have reported its function in SC proliferation and migration. This study found that Cyr61 protein is up-regulated after nerve injury, and Cyr61 secreted by SCs promotes motor neuron growth. Cyr61 could promote motor neuron growth through autocrine or paracrine mechanisms. Our study could contribute to understanding cellular and molecular mechanisms underlying SC’s support for neurons and may facilitate the regeneration of peripheral nerves after injury.
雪旺细胞(SCs)在周围神经修复中起着至关重要的作用。这是由于它们具有增殖、迁移和为轴突再生提供营养支持的能力。周围神经损伤时,SCs去分化和重编程以获得修复神经的能力。富半胱氨酸61 (Cyr61/CCN1)是基质细胞蛋白CCN家族的成员,我们已经报道了它在SC增殖和迁移中的作用。本研究发现,神经损伤后Cyr61蛋白表达上调,sc分泌Cyr61促进运动神经元生长。Cyr61可能通过自分泌或旁分泌机制促进运动神经元的生长。我们的研究有助于理解SC支持神经元的细胞和分子机制,并可能促进损伤后周围神经的再生。
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引用次数: 0
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