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Metabolites of native actinomycetes from Sof Umer cave reveal potent antimicrobial activity against selected pathogens in mice infection models sofumer洞穴天然放线菌的代谢物在小鼠感染模型中显示出对选定病原体的有效抗菌活性
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.ejbt.2025.100703
Ebisa Chaluma Abdeta , Abu Feyisa Meka , Daniel Girma Hordofa , Belete Ketema Sime , Gadisa Abdisa Akkewak , Jemal Ali Mahdi , Musin Kelel Abas , Mesfin Tafesse Gemeda

Background

Actinomycetes are gram-positive bacteria that belong to the actinobacterial species. They are a prolific source of secondary metabolites with various biological applications. Thus, this study aimed to culture-based isolation of potent Actinomycete species from Sof-Umer Cave and in vitro and in vivo evaluation of their potential metabolites against selected test organisms.

Result

Among the total isolates, ten isolates were selected based on their antimicrobial activities. Among them, the ethyl acetate crude extract of three isolates (RO13, SD2, R011) showed potential antagonistic activity, ranging from 17 ± 0.78 to 23 ± 0.56 mm of zone of inhibition against Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus aureus. Additionally, two isolates’ (SD2, R011) crude extract exhibited significant inhibition of test organisms in wound and oral infection of the mice models. This was confirmed by wound contraction and progress improvement of the clinical sign observed before treatment. Characterization of their crude extract by FTIR and GC–MS revealed the presence of various functional groups and compounds. Specifically, potent antimicrobial and antioxidant bioactive compounds, such as pyrrolo[1,2-a]pyrazine-1,4-dione, hexahydro-2-piperidine, phenol, 2-methoxy-4-(1-propenyl)-, and indolizine, were identified via GC–MS analysis. Three of the ten potent isolates (R013, R011, and SD2) were identified based on the 16S rRNA gene sequence, and the R013 isolate belongs to Streptomycetes flavoviridis, whereas SD2 and R011 were identified as Arthrobacter sp. and Actinobacterium kmd_152, respectively.

Conclusions

Sof-Umer cave-dwelling actinomycetes possess potent metabolites against test organisms that can be a base for future potent drug development against microbial infections.
How to cite: Abdeta EC, Meka AF, Hordofa DG, et al. Metabolites of native actinomycetes from Sof Umer cave reveal potent antimicrobial activity against selected pathogens in mice infection models. Electron J Biotechnol 2026;79. https://doi.org/10.1016/j.ejbt.2025.100703.
放线菌是革兰氏阳性细菌,属于放线菌属。它们是次生代谢物的丰富来源,具有多种生物学应用。因此,本研究旨在以培养为基础,从sofumer洞穴中分离出强效放线菌,并在体外和体内评估其对选定试验生物的潜在代谢物。结果根据抑菌活性筛选出10株。其中,3株菌株(RO13、SD2、R011)乙酸乙酯粗提物对大肠杆菌、铜绿假单胞菌和金黄色葡萄球菌的抑菌带范围为17±0.78 ~ 23±0.56 mm,表现出潜在的拮抗活性。此外,两株分离物(SD2, R011)粗提物对小鼠模型的伤口和口腔感染有明显的抑制作用。治疗前观察到的伤口收缩和临床症状的进展改善证实了这一点。通过FTIR和GC-MS对其粗提物进行表征,发现其含有多种官能团和化合物。具体来说,通过GC-MS分析鉴定出了有效的抗菌和抗氧化生物活性化合物,如吡咯[1,2-a]吡嗪-1,4-二酮、六氢-2-哌啶、苯酚、2-甲氧基-4-(1-丙烯基)-和吲哚嗪。根据16S rRNA基因序列鉴定出10株强效菌株中的3株(R013、R011和SD2),其中R013属于黄病毒链霉菌,而SD2和R011分别属于节杆菌sp.和放线菌kmd_152。结论sofo - umer穴居放线菌具有较强的抗微生物代谢产物,可为今后开发抗微生物感染药物奠定基础。如何引用:Abdeta EC, Meka AF, Hordofa DG等。sofumer洞穴天然放线菌的代谢物在小鼠感染模型中显示出对选定病原体的有效抗菌活性。中国生物医学工程学报(英文版);2009;https://doi.org/10.1016/j.ejbt.2025.100703。
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引用次数: 0
HRMS-based profiling of metabolites, metal ions content and in-vitro cholinesterase inhibitory activities of Sonchus wightianus DC plant parts 基于hrms的白松子植物代谢产物、金属离子含量及体外胆碱酯酶抑制活性分析
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-12-08 DOI: 10.1016/j.ejbt.2025.100702
Abhimat Subedi , Bishnu Prasad Pandey , Suman Prakash Pradhan , G.C. Ashok , Sumit Bhattarai , Ankita Dahal , Era Tuladhar , Anupama Chapagain , Mukti Ram Aryal , Gopal Prasad Ghimire

Background

Sonchus wightianus DC is native to South Asia and has traditionally been known for its wide range of applications for the treatment of several human ailments. However, its application for the treatment of neurodegenerative diseases like Alzheimer’s disease (AD) has not been studied yet. In this present study, comprehensive metabolite profiling of plant parts and in-vitro cholinesterase inhibitory potential was examined to see the efficacy of plant extract against AD.

Results

The potent antioxidant activity was demonstrated by the flower extract in both DPPH and ABTS assays, with IC50 values of 104.06 ± 2.05 µg/mL and 67.69 ± 1.58 µg/mL, respectively. The crude methanol extract of the leaf displayed the highest butyrylcholinesterase (BChE) inhibition potential with IC50 values of 281.09 ± 14.64 µg/mL. In contrast, the flower extract exhibited the strongest acetylcholinesterase (AChE) inhibition with IC50 values of 247.51 ± 11.15 µg/mL. Furthermore, the evaluated plant parts were a rich source of essential macro and micronutrients. Principal component analysis revealed the major contribution of total phenolic content (TPC), and total flavonoid content (TFC) in the plant extracts, which might be the prime reason for strong antioxidant and cholinesterase inhibition. Further, the HRMS profiling analysis revealed the presence of Linoleic acid, gingerol, kaempferol, genistein, daidzein, chlorogenic acid, fisetin and 12-oxo-phytodienoic acid.

Conclusions

The findings of this study suggest that Sonchus wightianus DC is a promising source of bioactive compounds and essential micronutrients, with notable potential as an anticholinesterase agent.
How to cite: Subedi A, Pandey BP, Pradhan SP, et al. HRMS-based profiling of metabolites, metal ions content and in-vitro cholinesterase inhibitory activities of Sonchus wightianus DC plant parts. Electron J Biotechnol 2026;79. https://doi.org/10.1016/j.ejbt.2025.100702.
sonchus wightianus DC原产于南亚,传统上因其广泛应用于治疗几种人类疾病而闻名。然而,其在治疗阿尔茨海默病(AD)等神经退行性疾病方面的应用尚未得到研究。在本研究中,研究了植物部位的综合代谢物谱和体外胆碱酯酶抑制潜力,以观察植物提取物对AD的疗效。结果花提取物在DPPH和ABTS实验中均表现出较强的抗氧化活性,IC50值分别为104.06±2.05µg/mL和67.69±1.58µg/mL。粗甲醇提取物对丁基胆碱酯酶(BChE)的抑制作用最强,IC50值为281.09±14.64µg/mL。相比之下,花提取物对乙酰胆碱酯酶(AChE)的抑制作用最强,IC50值为247.51±11.15µg/mL。此外,所评价的植物部位是必需宏量和微量营养素的丰富来源。主成分分析表明,总酚含量(TPC)和总黄酮含量(TFC)对植物提取物的抗氧化作用和胆碱酯酶抑制作用起主要作用。此外,HRMS分析还发现了亚油酸、姜辣素、山奈酚、染料木素、大豆苷元、绿原酸、非西汀和12-氧-植物二烯酸。结论白松子是一种很有潜力的生物活性化合物和必需微量营养素的来源,具有抗胆碱酯酶的潜力。如何引用:Subedi A, Pandey BP, Pradhan SP等。基于hrms的白松子植物代谢产物、金属离子含量及体外胆碱酯酶抑制活性分析中国生物医学工程学报(英文版);2009;https://doi.org/10.1016/j.ejbt.2025.100702。
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引用次数: 0
Anoikis- and m6A-related lncRNA analysis to identify prognostic indicators in liver hepatocellular carcinoma Anoikis-和m6a相关lncRNA分析鉴定肝癌预后指标
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-12-05 DOI: 10.1016/j.ejbt.2025.100701
Pan Yu , Shuaiyang Jing , Sarinder Kaur Dhillon

Background

In cancer, the process of anoikis is intimately associated with the emergence and progression. N6-methyladenosine modification and m6A modification play an important role in regulating long non-coding RNAs. The liver hepatocellular carcinoma patients’ data, including clinical and prognostic data, were obtained via The Cancer Genome Atlas database. The univariate, multivariate Cox and Least Absolute Selection Operator (LASSO) regression were performed to gain anoikis- and m6A-related lncRNAs. The Kaplan-Meier method was employed to assess the overall survival rate for groups of high- and low risks.

Results

A signature comprising six anoikis- and m6A-related lncRNAs was constructed: AL117336.3, LINC01138, Z83851.1, NRAV, CASC19 and AC009283.1. The clinicopathological variables, the anoikis- and m6A-related lncRNA signature demonstrated superior diagnostic efficacy, with an area under the receiver operating characteristic curve of 0.810. In the high-risk group, the overall survival was shown to be inferior to that of in group of low risk, while patients were classified by distinct clinicopathological variables. The ssGSEA and CIBERSORT immune analysis demonstrated that the predictive signature was significantly associated with liver cancer patients’ immune status. The chemotherapy drugs ATRA, AUY922, bexarotene, gemcitabine, mitomycin-C, and PHA have been found to have greater sensitivity in treating high-risk patients. qRT-PCR showed that Z83851.1, NRAV and CASC19 lncRNAs were associated with poor prognosis and were high-risk factors. AC009283.1 lncRNA may have anti-cancer properties.

Conclusions

The predictive signature is capable of independently predicting the prognosis of liver cancer patients for understanding the mechanisms of anoikis- and m6A-related lncRNAs in liver hepatocellular carcinoma and offering clinical guidance to patients with liver cancer.
How to cite: Yu P, Jing S, Dhillon SK. Anoikis and m6A related lncRNAs analysis to identify prognostic indicators in liver hepatocellular carcinoma. Electron J Biotechnol 2026;79. https://doi.org/10.1016/j.ejbt.2025.100701.
在癌症中,肿瘤的发生与发展密切相关。n6 -甲基腺苷修饰和m6A修饰在长链非编码rna调控中发挥重要作用。通过The Cancer Genome Atlas数据库获取肝细胞癌患者的临床和预后数据。采用单因素、多因素Cox和最小绝对选择算子(LASSO)回归获得anoikis和m6a相关的lncrna。Kaplan-Meier法用于评估高、低风险组的总生存率。结果构建了由6个anoikis和m6a相关lncrna组成的特征图谱:AL117336.3、LINC01138、Z83851.1、NRAV、CASC19和AC009283.1。临床病理变量anoikis-和m6a相关的lncRNA特征表现出较好的诊断效能,其在受试者工作特征曲线下的面积为0.810。高危组患者的总生存率明显低于低危组,而患者的临床病理指标不同。ssGSEA和CIBERSORT免疫分析表明,预测特征与肝癌患者的免疫状态显著相关。化疗药物ATRA、AUY922、贝沙罗汀、吉西他滨、丝裂霉素- c、PHA在治疗高危患者中具有较高的敏感性。qRT-PCR显示Z83851.1、NRAV和CASC19 lncrna与预后不良相关,为高危因素。AC009283.1 lncRNA可能具有抗癌特性。结论该预测特征能够独立预测肝癌患者的预后,有助于了解anoikis-和m6a相关lncrna在肝癌中的作用机制,为肝癌患者提供临床指导。Yu P, Jing S, Dhillon SK. Anoikis和m6A相关lncRNAs分析在肝细胞癌中的预后指标。中国生物医学工程学报(英文版);2009;https://doi.org/10.1016/j.ejbt.2025.100701。
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引用次数: 0
Low-cost hybrid copper–carbon nanotube coating with antimicrobial properties in ambient conditions 环境条件下具有抗菌性能的低成本杂化铜碳纳米管涂层
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-12-04 DOI: 10.1016/j.ejbt.2025.100700
Christian Pablo Romero , Claudio Ramirez-Mora , Rodolfo Salazar , Cristobal Fernandez , Cristian Acevedo , Christian Orellana , Maria Abellan , David Aliaga

Background

The development of bactericidal surfaces using nanotechnology has gained traction in high-tech sectors due to their effectiveness against pathogens. However, widespread adoption in low-income regions remains limited by the high cost of materials such as copper nanoparticles and the need for specialized application personnel. This study aims to develop a cost-effective bactericidal coating that minimizes nano-copper usage while maintaining strong antimicrobial performance and practical applicability in resource-limited environments.

Results

A polymer-based coating incorporating ≤3 wt% nano-copper and carbon nanotubes was formulated to enhance conductivity and mechanical stability. The fabrication process was optimized for on-site application under ambient conditions. Scanning Electron Microscopy (SEM) revealed a uniform surface distribution of nano-copper particles. Bactericidal activity tests confirmed efficacy against Escherichia coli, Listeria monocytogenes, and Salmonella spp. Techno-economic analysis indicated that the coating could be integrated into existing surface finishing systems at an incremental cost of 2.6–3.5 USD per gallon.

Conclusions

This work demonstrates the feasibility of producing and applying affordable nano-based bactericidal coatings under real-world conditions. The approach provides a practical pathway for implementing antimicrobial surface technologies in low-resource settings. Although the present study focused on wood substrates, future research should assess performance on diverse materials to broaden applicability. The combination of cost-effectiveness, efficacy, and scalability underscores the potential for both commercial adoption and significant public health benefits.
How to cite: Romero CP, Ramirez-Mora C, Salazar R, et al. Low-cost hybrid copper–carbon nanotube coating with antimicrobial properties in ambient conditions. Electron J Biotechnol 2026;79. https://doi.org/10.1016/j.ejbt.2025.100700.
利用纳米技术开发杀菌表面由于其对病原体的有效性而在高科技领域得到了发展。然而,在低收入地区的广泛采用仍然受到诸如铜纳米颗粒等材料的高成本和对专业应用人员的需求的限制。本研究旨在开发一种具有成本效益的杀菌涂层,最大限度地减少纳米铜的使用,同时在资源有限的环境中保持强大的抗菌性能和实用性。结果制备了纳米铜和碳纳米管含量≤3wt %的聚合物基涂层,提高了涂层的导电性和机械稳定性。对制造工艺进行了优化,以适应环境条件下的现场应用。扫描电子显微镜(SEM)显示纳米铜颗粒表面分布均匀。杀菌活性测试证实了对大肠杆菌、单核细胞增多李斯特菌和沙门氏菌的杀菌效果。技术经济分析表明,该涂层可以集成到现有的表面处理系统中,每加仑的增量成本为2.6-3.5美元。结论本工作证明了在实际条件下生产和应用价格合理的纳米基杀菌涂料的可行性。该方法为在低资源环境中实施抗菌表面技术提供了切实可行的途径。虽然目前的研究主要集中在木材基材上,但未来的研究应评估不同材料的性能,以扩大适用性。成本效益、功效和可扩展性的结合突出了商业采用和重大公共卫生效益的潜力。如何引用:Romero CP, Ramirez-Mora C, Salazar R等。环境条件下具有抗菌性能的低成本杂化铜碳纳米管涂层。中国生物医学工程学报(英文版);2009;https://doi.org/10.1016/j.ejbt.2025.100700。
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引用次数: 0
Can broad bean (Vicia faba) and white lupin (Lupinus albus) flours serve as carbon sources to support probiotic growth? 蚕豆(Vicia faba)和白露宾(Lupinus albus)面粉可以作为碳源来支持益生菌的生长吗?
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-11-27 DOI: 10.1016/j.ejbt.2025.100697
Evla Vieira, Marta W. Vasconcelos, Ana Maria Gomes

Background

There is growing interest in identifying substrates that support the growth of probiotics in foods. Pulses are an excellent source of nutrients and bioactive compounds, including non-digestible oligosaccharides from the α-galactoside group, which are probiotic growth factors. This study aimed to evaluate the potential of white lupin and broad bean flours to support the growth of seven probiotic strains of Lactobacilli and Bifidobacterium.

Results

Different Man-Rogosa-Sharpe broth media were prepared using whole or dehulled flour as carbon sources at different concentrations (20, 30, 40, and 60 g/L) and inoculated with 2% (w/v) of each probiotic strain. Viable cell numbers and medium acidification were monitored throughout fermentation and compared to negative (MRS without a carbon source) and positive (MRS with 20 g/L glucose) controls. White lupin at 60 g/L concentration proved to be a suitable carbon source for both Lactobacillus acidophilus Ki and Lactobacillus casei ssp. paracasei L26, while concentrations of 40 g/L and 60 g/L supported Bifidobacterium animalis Bb12 growth.

Conclusions

Flour concentration had a greater impact on probiotic growth than composition (hull vs. dehulled). These results suggested that white lupin is a promising ingredient for the development of functional foods.
How to cite: Vieira E, Vasconcelos MW, Gomes AM. Can broad bean (Vicia faba) and white lupin (Lupinus albus) flours serve as carbon sources to support probiotic growth? Electron J Biotechnol 2026;5;79. https://doi.org/10.1016/j.ejbt.2025.100697.
人们对确定食物中支持益生菌生长的底物越来越感兴趣。豆类是营养物质和生物活性化合物的极好来源,包括α-半乳糖苷群中不可消化的低聚糖,这是益生菌生长因子。本研究旨在评价白豆粉和蚕豆粉对乳酸菌和双歧杆菌7株益生菌生长的支持作用。结果以全面粉和去皮面粉为碳源,分别以20、30、40和60 g/L的碳源配制不同的Man-Rogosa-Sharpe培养基,每种益生菌接种量为2% (w/v)。在整个发酵过程中监测活细胞数量和培养基酸化情况,并与阴性(无碳源的MRS)和阳性(含20 g/L葡萄糖的MRS)对照进行比较。结果表明,60 g/L浓度的白露菇是嗜酸乳杆菌和干酪乳杆菌适宜的碳源。而40 g/L和60 g/L的浓度支持动物双歧杆菌Bb12的生长。结论面粉浓度对益生菌生长的影响大于面粉组成(去皮与去皮)。这些结果表明,白露是一种很有前景的功能性食品原料。引文来源:Vieira E, Vasconcelos MW, Gomes AM。蚕豆(Vicia faba)和白露宾(Lupinus albus)面粉可以作为碳源来支持益生菌的生长吗?中国生物医学工程学报(英文版);2009;5;79。https://doi.org/10.1016/j.ejbt.2025.100697。
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引用次数: 0
Obituary for James D. Watson (1928–2025) 詹姆斯·d·沃森讣告(1928-2025)
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-11-25 DOI: 10.1016/j.ejbt.2025.100699
Graciela Muñoz-Riveros
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引用次数: 0
Biogenic synthesis of silver nanoparticles using cell-free extracts of thermotolerant bacteria: Antioxidant and antibacterial properties 利用耐热细菌的无细胞提取物生物合成纳米银:抗氧化和抗菌性能
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-11-23 DOI: 10.1016/j.ejbt.2025.100698
Aparna Banerjee , Ismael Herrera-Vargas , Mario E. Flores , Francisca Valenzuela , Srijan Banerjee

Background

Eco-friendly synthesis of silver nanoparticles (AgNPs) using biological systems offers a sustainable alternative to conventional physicochemical methods. In this study, we employed cell-free extracts from three thermotolerant bacterial strains, Bacillus haynesii CamB6, Pseudomonas alcaligenes Med1, and Staphylococcus sp. BSP3 for the biosynthesis of AgNPs, aiming to explore their antioxidant and antibacterial properties.

Results

The biosynthesized AgNPs were characterized through UV–Vis spectroscopy, FTIR, TEM, and DLS analyses, which revealed distinct physicochemical profiles among the nanoparticles. Notably, AgNP2 and AgNP3 exhibited smaller particle sizes, enhanced colloidal stability, and superior biological activities compared to AgNP1. Antioxidant evaluation demonstrated significant free radical scavenging potential, with AgNP2 showing the highest DPPH activity (65.18% at 5 mg mL−1). Antibacterial activity, assessed via agar well diffusion and cell viability assays against Bacillus cereus and Pseudomonas putida revealed that AgNP2 achieved the lowest bacterial viability (0.74%) for P. putida at 1 mg mL−1 concentration.

Conclusions

The study highlights the potential of biosynthesized AgNPs, particularly AgNP2, as sustainable for biomedical applications. Their antioxidant and antibacterial activities suggest valuable applications in managing oxidative stress and combating antimicrobial resistance.
How to cite: Banerjee A, Herrera-Vargas I, Flores ME, et al. Biogenic synthesis of silver nanoparticles using cell-free extracts of thermotolerant bacteria: Antioxidant and antibacterial properties. Electron J Biotechnol 2026:79. https://doi.org/10.1016/j.ejbt.2025.100698.
利用生物系统合成银纳米颗粒(AgNPs)为传统的物理化学方法提供了一种可持续的选择。本研究利用haynesii CamB6、Pseudomonas alcaligenes Med1和Staphylococcus sp. BSP3三种耐热菌株的无细胞提取物进行AgNPs的生物合成,探讨AgNPs的抗氧化和抗菌性能。结果通过紫外可见光谱(UV-Vis)、红外光谱(FTIR)、透射电镜(TEM)和能谱分析(DLS)对合成的AgNPs进行了表征。值得注意的是,与AgNP1相比,AgNP2和AgNP3具有更小的粒径、更强的胶体稳定性和更优越的生物活性。抗氧化评价显示出显著的自由基清除潜力,AgNP2显示出最高的DPPH活性(在5 mg mL−1时为65.18%)。通过琼脂孔扩散和对蜡样芽孢杆菌和恶臭假单胞菌的抑菌活性测定,AgNP2在1 mg mL−1浓度下对恶臭假单胞菌的抑菌活性最低(0.74%)。该研究强调了生物合成AgNPs,特别是AgNP2在生物医学应用方面的可持续潜力。它们的抗氧化和抗菌活性在处理氧化应激和对抗抗菌素耐药性方面具有重要的应用价值。如何引用:Banerjee A, Herrera-Vargas I, Flores ME等。利用耐热细菌的无细胞提取物生物合成纳米银:抗氧化和抗菌性能。电子学报[J] . 2026(6): 779。https://doi.org/10.1016/j.ejbt.2025.100698。
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引用次数: 0
ANKRD1 knockdown attenuates doxorubicin-induced dilated cardiomyopathy by regulating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway ANKRD1敲低可通过激活AMPK/AKT/mTOR通路调节线粒体功能障碍和氧化应激,从而减轻阿霉素诱导的扩张型心肌病
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-11-11 DOI: 10.1016/j.ejbt.2025.08.002
Jia Yuan , Yu Zhou , GuoHua Wei , Tao Qi , HaoLiang Sun , Jian Shen

Background

Doxorubicin (DOX), a widely used chemotherapeutic agent, causes severe cardiotoxicity that frequently progresses to dilated cardiomyopathy (DCM). While ankyrin repeat domain 1 protein (ANKRD1) plays critical roles in cardiovascular pathophysiology, its specific involvement in doxorubicin-induced DCM remains unknown. This study investigates the functional significance of ANKRD1 in DOX-induced DCM pathogenesis.

Results

DOX treatment significantly upregulated ANKRD1 expression in both rat models and H9c2 rat cardiomyocytes. In vivo, ANKRD1 knockdown ameliorated DOX-induced cardiac dysfunction, as demonstrated by improved left ventricular ejection fraction and fractional shortening, along with reduced serum levels of lactate dehydrogenase and creatine kinase-myocardial band. Conversely, ANKRD1 overexpression exacerbated cardiac impairment. Pathological examination revealed that ANKRD1 knockdown attenuated DOX-induced myocardial tissue damage and collagen deposition, while ANKRD1 overexpression intensified these pathological changes. Furthermore, ANKRD1 knockdown mitigated mitochondrial dysfunction and oxidative stress in DCM models both in vivo and in vitro. Mechanistically, ANKRD1 knockdown activated the AMP-activated protein kinase (AMPK)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling cascade, thereby attenuating DOX-induced cardiomyocyte toxicity, mitochondrial dysfunction, and oxidative stress. Rescue experiments using the AMPK inhibitor dorsomorphin confirmed this pathway’s involvement, as dorsomorphin treatment abolished the protective effects of ANKRD1 knockdown against DOX-induced cardiomyocyte damage.

Conclusions

ANKRD1 knockdown prevents DOX-induced DCM by ameliorating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway. These findings establish ANKRD1 as a promising therapeutic target for preventing DOX-induced cardiotoxicity and DCM.
How to cite: Yuan J, Zhou Y, Wei G, et al. ANKRD1 knockdown attenuates doxorubicin-induced dilated cardiomyopathy by regulating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway. Electron J Biotechnol 2026, 79. https://doi.org/10.1016/j.ejbt.2025.08.002.
多柔比星(DOX)是一种广泛使用的化疗药物,可引起严重的心脏毒性,经常发展为扩张型心肌病(DCM)。虽然锚蛋白重复结构域1蛋白(ANKRD1)在心血管病理生理中起关键作用,但其在阿霉素诱导的DCM中的具体参与尚不清楚。本研究探讨ANKRD1在dox诱导的DCM发病机制中的功能意义。结果dox处理显著上调ANKRD1在模型大鼠和H9c2大鼠心肌细胞中的表达。在体内,ANKRD1敲低可改善dox诱导的心功能障碍,如左心室射血分数和分数缩短的改善,以及血清乳酸脱氢酶和肌酸激酶-心肌带水平的降低。相反,ANKRD1过表达加重了心脏损害。病理检查显示,ANKRD1敲低可减轻dox诱导的心肌组织损伤和胶原沉积,而ANKRD1过表达可增强这些病理改变。此外,ANKRD1敲低可减轻体内和体外DCM模型的线粒体功能障碍和氧化应激。在机制上,ANKRD1敲低激活了amp激活的蛋白激酶(AMPK)/蛋白激酶B (AKT)/哺乳动物雷帕霉素靶点(mTOR)信号级联,从而减轻dox诱导的心肌细胞毒性、线粒体功能障碍和氧化应激。使用AMPK抑制剂dorsomorphin的救援实验证实了这一途径的参与,因为dorsomorphin治疗消除了ANKRD1敲低对dox诱导的心肌细胞损伤的保护作用。结论sankrd1敲低可通过激活AMPK/AKT/mTOR通路改善线粒体功能障碍和氧化应激,从而预防dox诱导的DCM。这些发现表明ANKRD1是预防dox诱导的心脏毒性和DCM的有希望的治疗靶点。引用方式:袁杰,周勇,魏刚,等。ANKRD1敲低可通过激活AMPK/AKT/mTOR通路调节线粒体功能障碍和氧化应激,从而减轻阿霉素诱导的扩张型心肌病。中国生物医学工程学报,2016,33(2):444 - 444。https://doi.org/10.1016/j.ejbt.2025.08.002。
{"title":"ANKRD1 knockdown attenuates doxorubicin-induced dilated cardiomyopathy by regulating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway","authors":"Jia Yuan ,&nbsp;Yu Zhou ,&nbsp;GuoHua Wei ,&nbsp;Tao Qi ,&nbsp;HaoLiang Sun ,&nbsp;Jian Shen","doi":"10.1016/j.ejbt.2025.08.002","DOIUrl":"10.1016/j.ejbt.2025.08.002","url":null,"abstract":"<div><h3>Background</h3><div>Doxorubicin (DOX), a widely used chemotherapeutic agent, causes severe cardiotoxicity that frequently progresses to dilated cardiomyopathy (DCM). While ankyrin repeat domain 1 protein (ANKRD1) plays critical roles in cardiovascular pathophysiology, its specific involvement in doxorubicin-induced DCM remains unknown. This study investigates the functional significance of ANKRD1 in DOX-induced DCM pathogenesis.</div></div><div><h3>Results</h3><div>DOX treatment significantly upregulated ANKRD1 expression in both rat models and H9c2 rat cardiomyocytes. <em>In vivo</em>, ANKRD1 knockdown ameliorated DOX-induced cardiac dysfunction, as demonstrated by improved left ventricular ejection fraction and fractional shortening, along with reduced serum levels of lactate dehydrogenase and creatine kinase-myocardial band. Conversely, ANKRD1 overexpression exacerbated cardiac impairment. Pathological examination revealed that ANKRD1 knockdown attenuated DOX-induced myocardial tissue damage and collagen deposition, while ANKRD1 overexpression intensified these pathological changes. Furthermore, ANKRD1 knockdown mitigated mitochondrial dysfunction and oxidative stress in DCM models both <em>in vivo</em> and <em>in vitro</em>. Mechanistically, ANKRD1 knockdown activated the AMP-activated protein kinase (AMPK)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling cascade, thereby attenuating DOX-induced cardiomyocyte toxicity, mitochondrial dysfunction, and oxidative stress. Rescue experiments using the AMPK inhibitor dorsomorphin confirmed this pathway’s involvement, as dorsomorphin treatment abolished the protective effects of ANKRD1 knockdown against DOX-induced cardiomyocyte damage.</div></div><div><h3>Conclusions</h3><div>ANKRD1 knockdown prevents DOX-induced DCM by ameliorating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway. These findings establish ANKRD1 as a promising therapeutic target for preventing DOX-induced cardiotoxicity and DCM.</div><div><strong>How to cite:</strong> Yuan J, Zhou Y, Wei G, et al. ANKRD1 knockdown attenuates doxorubicin-induced dilated cardiomyopathy by regulating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway. Electron J Biotechnol 2026, 79. <span><span>https://doi.org/10.1016/j.ejbt.2025.08.002</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"79 ","pages":"Article 100696"},"PeriodicalIF":2.5,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145749970","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
Kaixin San in treating vascular dementia via regulating the Bcl-2/Beclin-1/LC3A/B signaling pathway via animal experiments and network pharmacology analysis 动物实验及网络药理学分析表明开心散通过调节Bcl-2/Beclin-1/LC3A/B信号通路治疗血管性痴呆
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-11-01 DOI: 10.1016/j.ejbt.2025.08.001
Meng-qi Li , Yu-cheng Lu , Yan-chun Li , Yu-fu Zeng , Ying-ying Cao , Ling Zhang , Ben Chen , Ling Chen , Wei-an Qiu , Zi-heng Huang

Background

Kaixin San (KXS), a traditional Chinese herbal formula, is used to treat vascular dementia (VaD), but its active ingredients and mechanisms remain unclear. This study combined animal experiments with network pharmacology to explore how KXS modulates the Bcl-2/Beclin-1/LC3A/B pathway in VaD treatment.

Results

LC‒MS/MS identified 164 active ingredients in the KXS ethanol extract. In 2-vessel occlusion model rats, KXS significantly improved learning and memory (p < 0.05 or p < 0.01) and reduced hippocampal CA1 neuronal damage. Western blotting showed KXS upregulated Bcl-2/Bcl-XL and downregulated Beclin-1, LC3A/B, and Bax (p < 0.05). Immunofluorescence confirmed increased Bcl-2 and decreased Beclin-1 expression. Network pharmacology predicted 73 targets and 174 pathways, with TNF, AKT1, IL-1β, PTGS2, and ESR1 as key targets. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis linked these targets to cancer, atherosclerosis, and AGE-RAGE signaling pathways.

Conclusions

KXS alleviates VaD by modulating autophagy and apoptosis via Bcl-2/Beclin-1/LC3A/B, with multi-target, multi-pathway effects. These findings support further investigation of KXS as a potential therapy for VaD.
How to cite: Li M, Lu Y, Li Y, et al. Kaixin San in treating vascular dementia via regulating the Bcl-2/Beclin-1/LC3A/B signaling pathway via animal experiments and network pharmacology analysis. Electron J Biotechnol 2025;78. https://doi.org/10.1016/j.ejbt.2025.08.001.
开心散(KXS)是一种治疗血管性痴呆(VaD)的传统中药配方,但其有效成分和作用机制尚不清楚。本研究将动物实验与网络药理学相结合,探讨KXS如何调节Bcl-2/Beclin-1/LC3A/B通路在VaD治疗中的作用。结果薄层色谱-质谱联用技术鉴定出了164种有效成分。两支血管闭塞模型大鼠,KXS显著改善学习记忆(p <; 0.05或p <; 0.01),减轻海马CA1神经元损伤。Western blotting显示KXS上调Bcl-2/Bcl-XL,下调Beclin-1、LC3A/B和Bax (p < 0.05)。免疫荧光证实Bcl-2表达升高,Beclin-1表达降低。网络药理学预测73个靶点和174条通路,其中TNF、AKT1、IL-1β、PTGS2和ESR1是关键靶点。京都基因和基因组百科全书(KEGG)分析将这些靶点与癌症、动脉粥样硬化和AGE-RAGE信号通路联系起来。结论skxs通过Bcl-2/Beclin-1/LC3A/B调控VaD的自噬和凋亡,具有多靶点、多通路的作用。这些发现支持进一步研究KXS作为VaD的潜在治疗方法。引用方式:李敏,陆毅,李毅,等。动物实验及网络药理学分析表明开心散通过调节Bcl-2/Beclin-1/LC3A/B信号通路治疗血管性痴呆。中国生物医学工程学报(英文版);2009;38。https://doi.org/10.1016/j.ejbt.2025.08.001。
{"title":"Kaixin San in treating vascular dementia via regulating the Bcl-2/Beclin-1/LC3A/B signaling pathway via animal experiments and network pharmacology analysis","authors":"Meng-qi Li ,&nbsp;Yu-cheng Lu ,&nbsp;Yan-chun Li ,&nbsp;Yu-fu Zeng ,&nbsp;Ying-ying Cao ,&nbsp;Ling Zhang ,&nbsp;Ben Chen ,&nbsp;Ling Chen ,&nbsp;Wei-an Qiu ,&nbsp;Zi-heng Huang","doi":"10.1016/j.ejbt.2025.08.001","DOIUrl":"10.1016/j.ejbt.2025.08.001","url":null,"abstract":"<div><h3>Background</h3><div>Kaixin San (KXS), a traditional Chinese herbal formula, is used to treat vascular dementia (VaD), but its active ingredients and mechanisms remain unclear. This study combined animal experiments with network pharmacology to explore how KXS modulates the Bcl-2/Beclin-1/LC3A/B pathway in VaD treatment.</div></div><div><h3>Results</h3><div>LC‒MS/MS identified 164 active ingredients in the KXS ethanol extract. In 2-vessel occlusion model rats, KXS significantly improved learning and memory (<em>p</em> &lt; 0.05 or <em>p</em> &lt; 0.01) and reduced hippocampal CA1 neuronal damage. Western blotting showed KXS upregulated Bcl-2/Bcl-XL and downregulated Beclin-1, LC3A/B, and Bax (<em>p</em> &lt; 0.05). Immunofluorescence confirmed increased Bcl-2 and decreased Beclin-1 expression. Network pharmacology predicted 73 targets and 174 pathways, with TNF, AKT1, IL-1β, PTGS2, and ESR1 as key targets. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis linked these targets to cancer, atherosclerosis, and AGE-RAGE signaling pathways.</div></div><div><h3>Conclusions</h3><div>KXS alleviates VaD by modulating autophagy and apoptosis via Bcl-2/Beclin-1/LC3A/B, with multi-target, multi-pathway effects. These findings support further investigation of KXS as a potential therapy for VaD.</div><div><strong>How to cite:</strong> Li M, Lu Y, Li Y, et al. Kaixin San in treating vascular dementia via regulating the Bcl-2/Beclin-1/LC3A/B signaling pathway via animal experiments and network pharmacology analysis. Electron J Biotechnol 2025;78. <span><span>https://doi.org/10.1016/j.ejbt.2025.08.001</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"78 ","pages":"Pages 96-109"},"PeriodicalIF":2.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145413009","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
METTL16 promotes osteosarcoma progression by inducing m6A methylation of the UBE3A and Notch signaling pathway METTL16通过诱导UBE3A和Notch信号通路的m6A甲基化来促进骨肉瘤的进展
IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2025-10-09 DOI: 10.1016/j.ejbt.2025.07.006
Yanlin Tan , Jun Gao

Background

N6-methyladenosine (m6A) methylation plays a key role in osteosarcoma (OS) progression. This study aimed to elucidate the function and mechanism of methyltransferase 16 (METTL16), an m6A methyltransferase, in OS progression.

Results

Bioinformatics analysis with quantitative reverse-transcription polymerase chain reaction (qRT-PCR) revealed high METTL16 expression in OS. After performing cell functional experiments, METTL16 silencing was shown to decrease the proliferation, migration, and invasion of OS cells. Using qRT-PCR, methylated RNA immunoprecipitation quantitative polymerase chain reaction (MeRIP-qPCR), Western blotting, luciferase, RNA-binding protein immunoprecipitation (RIP), and RNA stability assays, METTL16 induced the m6A methylation of ubiquitin protein ligase E3A (UBE3A) to promote UBE3A expression and mRNA stability in OS cells in a fragile X messenger ribonucleoprotein 1 (FMR1)-dependent manner. Moreover, in vitro and in vivo results showed that UBE3A activated the Notch signaling pathway, thereby promoting OS cell malignancy. METTL16 knockdown partly reversed the oncogenic role of UBE3A in OS cells.

Conclusions

METTL16 acts as a tumor promotor in OS progression by modulating UBE3A expression via m6A methylation to activate the Notch signaling pathway. The findings highlight the therapeutic potential of disrupting the METTL16–UBE3A–Notch pathway axis in OS.
How to cite: Tan Y, Gao J. METTL16 promotes osteosarcoma progression by inducing m6A methylation of the UBE3A and Notch signaling pathway. Electron J Biotechnol 2025;78. https://doi.org/10.1016/j.ejbt.2025.07.006.
n6 -甲基腺苷(m6A)甲基化在骨肉瘤(OS)的进展中起关键作用。本研究旨在阐明m6A甲基转移酶甲基转移酶16 (methyltransferase 16, METTL16)在OS进展中的作用和机制。结果定量逆转录聚合酶链反应(qRT-PCR)生物信息学分析显示METTL16在OS中高表达。细胞功能实验表明,METTL16沉默可降低OS细胞的增殖、迁移和侵袭。通过qRT-PCR、甲基化RNA免疫沉淀定量聚合酶链反应(MeRIP-qPCR)、Western blotting、荧光素酶、RNA结合蛋白免疫沉淀(RIP)和RNA稳定性分析,METTL16诱导泛素蛋白连接酶E3A (UBE3A)的m6A甲基化,以脆性X信使核糖核蛋白1 (FMR1)依赖的方式促进UBE3A在OS细胞中的表达和mRNA稳定性。此外,体外和体内实验结果表明,UBE3A激活Notch信号通路,从而促进OS细胞恶性。METTL16敲低部分逆转了UBE3A在OS细胞中的致癌作用。结论smettl16通过m6A甲基化调节UBE3A表达激活Notch信号通路,在OS进展中发挥肿瘤启动子作用。这些发现强调了破坏METTL16-UBE3A-Notch通路轴在OS中的治疗潜力。METTL16通过诱导UBE3A和Notch信号通路的m6A甲基化促进骨肉瘤的进展。中国生物医学工程学报(英文版);2009;38。https://doi.org/10.1016/j.ejbt.2025.07.006。
{"title":"METTL16 promotes osteosarcoma progression by inducing m6A methylation of the UBE3A and Notch signaling pathway","authors":"Yanlin Tan ,&nbsp;Jun Gao","doi":"10.1016/j.ejbt.2025.07.006","DOIUrl":"10.1016/j.ejbt.2025.07.006","url":null,"abstract":"<div><h3>Background</h3><div>N6-methyladenosine (m<sup>6</sup>A) methylation plays a key role in osteosarcoma (OS) progression. This study aimed to elucidate the function and mechanism of methyltransferase 16 (METTL16), an m<sup>6</sup>A methyltransferase, in OS progression.</div></div><div><h3>Results</h3><div>Bioinformatics analysis with quantitative reverse-transcription polymerase chain reaction (qRT-PCR) revealed high METTL16 expression in OS. After performing cell functional experiments, METTL16 silencing was shown to decrease the proliferation, migration, and invasion of OS cells. Using qRT-PCR, methylated RNA immunoprecipitation quantitative polymerase chain reaction (MeRIP-qPCR), Western blotting, luciferase, RNA-binding protein immunoprecipitation (RIP), and RNA stability assays, METTL16 induced the m<sup>6</sup>A methylation of ubiquitin protein ligase E3A (UBE3A) to promote UBE3A expression and mRNA stability in OS cells in a fragile X messenger ribonucleoprotein 1 (FMR1)-dependent manner. Moreover, <em>in vitro</em> and <em>in vivo</em> results showed that UBE3A activated the Notch signaling pathway, thereby promoting OS cell malignancy. METTL16 knockdown partly reversed the oncogenic role of UBE3A in OS cells.</div></div><div><h3>Conclusions</h3><div>METTL16 acts as a tumor promotor in OS progression by modulating UBE3A expression via m<sup>6</sup>A methylation to activate the Notch signaling pathway. The findings highlight the therapeutic potential of disrupting the METTL16–UBE3A–Notch pathway axis in OS.</div><div><strong>How to cite:</strong> Tan Y, Gao J. METTL16 promotes osteosarcoma progression by inducing m6A methylation of the UBE3A and Notch signaling pathway. Electron J Biotechnol 2025;78. <span><span>https://doi.org/10.1016/j.ejbt.2025.07.006</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"78 ","pages":"Pages 86-95"},"PeriodicalIF":2.5,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145358090","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
期刊
Electronic Journal of Biotechnology
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