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Luteolin Inhibits Ferroptosis of HUVEC by Regulating the Sirt1/Nrf2 Pathway. 木犀草素通过调节Sirt1/Nrf2通路抑制HUVEC铁凋亡。
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-01 Epub Date: 2025-07-28 DOI: 10.1007/s12013-025-01831-1
Ming Xiang, Xiangdong Lin, Haiying Chen

Coronary heart disease (CHD) is a disease caused by organic and functional coronary artery stenosis, resulting in a reduced oxygen supply to the heart. This study aimed to investigate the mechanism via which Luteolin regulates the Sirt1/Nrf2 pathway to inhibit ferroptosis in human umbilical vein endothelial cells (HUVEC) associated with CHD. An ox-LDL-induced HUVEC cell model with Sirt1 silencing and Luteolin treatment was established. The silencing efficiency of Sirt1 was validated using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analysis. The results of molecular docking and DARTS experiments showed that Luteolin could effectively bind Sirt1. Subsequently, we measured the expression of Nrf2 and Sirt1, cell viability, MDA, GSH, Fe2+ levels, lipid ROS content, expression of ferroptosis-related proteins GPX4, FTH, FTL, and cell migration parameters. The results showed that Luteolin could activate the Sirt1/Nrf2 axis and effectively inhibit ox-LDL-induced ferroptosis in HUVEC. Experimental results revealed that Luteolin could enhance HUVEC cell viability, decrease MDA, Fe2+, and ROS levels, increase GSH levels, promote the expression of HO-1, GPX4, FTH, FTL, inhibit the expression of ACSL4 and TFRC, and enhance the migration capability of HUVEC cells. Moreover, silencing Sirt1 reversed the effects of Luteolin on the activation of Sirt1 and Nrf2, confirming the dependence of these effects on the Sirt1/Nrf2 signaling pathway. In conclusion, this study indicates that Luteolin could inhibit ferroptosis in HUVEC in CHD by modulating the Sirt1/Nrf2 axis, providing a basis for further research on strategies for preventing and treating CHD and related diseases.

冠心病(CHD)是一种由器质性和功能性冠状动脉狭窄引起的疾病,导致心脏供氧减少。本研究旨在探讨木犀草素通过调控Sirt1/Nrf2通路抑制冠心病相关人脐静脉内皮细胞(HUVEC)铁下沉的机制。建立ox- ldl诱导的Sirt1沉默和木犀草素处理的HUVEC细胞模型。通过定量逆转录聚合酶链反应(qRT-PCR)和Western blot分析验证Sirt1的沉默效率。分子对接和dart实验结果表明木犀草素能有效结合Sirt1。随后,我们测量了Nrf2和Sirt1的表达、细胞活力、MDA、GSH、Fe2+水平、脂质ROS含量、凋亡相关蛋白GPX4、FTH、FTL的表达以及细胞迁移参数。结果表明木犀草素可以激活Sirt1/Nrf2轴,有效抑制ox- ldl诱导的HUVEC铁凋亡。实验结果显示木草素可提高HUVEC细胞活力,降低MDA、Fe2+、ROS水平,升高GSH水平,促进HO-1、GPX4、FTH、FTL表达,抑制ACSL4、TFRC表达,增强HUVEC细胞迁移能力。此外,沉默Sirt1逆转了木犀草素对Sirt1和Nrf2激活的作用,证实了这些作用对Sirt1/Nrf2信号通路的依赖性。综上所述,本研究提示木犀草素可通过调节Sirt1/Nrf2轴抑制冠心病HUVEC中的铁凋亡,为进一步研究冠心病及相关疾病的防治策略提供依据。
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引用次数: 0
Energy Decomposition-Driven Design of Trop2-Targeting Peptide. 能量分解驱动的trop2靶向肽设计。
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-01 Epub Date: 2025-08-08 DOI: 10.1007/s12013-025-01866-4
Yu-Chao Meng, He Liu, Bi-Shao Sun, Hong-Yuan Liu, Hong-Wei Li, Qiu-Yu Liao, Mouxin Huang, Qin Ouyang
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引用次数: 0
Cytotoxicity and Antiplatelet Activity of Cationic Antimicrobial Peptides of the Medicinal Leech Hirudo Medicinalis. 药用水蛭水蛭阳离子抗菌肽的细胞毒性和抗血小板活性。
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-01 Epub Date: 2025-08-08 DOI: 10.1007/s12013-025-01860-w
Grigoriy D Moroz, Nadezhda A Podoplelova, Mikhail S Iudin, Sabina E Alieva, Anna M Varizhuk, Mikhail A Panteleev, Vassili N Lazarev, Oleg M Panasenko
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引用次数: 0
Flavonoid-Rich Extracts from Mentha Piperita and their Novel Role in ALT Modulation in a Cardiovascular Disease Rat Model. 薄荷类黄酮提取物及其在心血管疾病模型大鼠ALT调节中的新作用
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-11-27 DOI: 10.1007/s12013-025-01952-7
Nuha Ali Hadi Al-Samarrie, Huda Ghazi Naser, Suror A Mahdi, Rasha Saad Jwad, Mohammed Basil Anwer, Zamzam Alhuwaymil, Sohad A Alshareef, Mohammed S S Alyami, Mohammed H Al-Mashhadani, Great Iruoghene Edo
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引用次数: 0
CENPI Promotes the Progression in Oral Squamous Cell Carcinoma and Is Regulated by E2F4. CENPI促进口腔鳞状细胞癌的进展并受E2F4调控。
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-11-22 DOI: 10.1007/s12013-025-01938-5
Yi Chen, Fei Duan, Xinxing Duan, Xutao Wen, Xiong Yu, Dan Li
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引用次数: 0
The Dual Nature of Oncostatin M: Context-Dependent Mediator of Immunity and Fibrosis. 肿瘤抑制素M的双重性质:免疫和纤维化的环境依赖介质。
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-11-22 DOI: 10.1007/s12013-025-01954-5
Satyajit Tripathy
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引用次数: 0
Synergistic Regeneration of Osteoporotic Bone Defects Using PBM, Stem Cells, and hMPMS Scaffolds Via the miR-21/RUNX2 Axis. 通过miR-21/RUNX2轴使用PBM、干细胞和hMPMS支架协同再生骨质疏松性骨缺损
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-11-18 DOI: 10.1007/s12013-025-01948-3
Bahareh Fallah, Abdollah Amini, Atarodalsadat Mostafavinia, Paria Asgharnejad, Mahyar Mahdavi, Seyed Mohammadmisagh Moteshakereh, Parvin Mirzaei Seresht, Fatemeh Zare, Sufan Chien, Mohammad Bayat
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引用次数: 0
Green Synthesis of Platinum Nanoparticles Using Aqueous Broccoli Extract for Antimicrobial, Antioxidant, Wound Healing, Antidiabetic, and Anticancer Applications. 绿色合成纳米铂的水西兰花提取物抗菌,抗氧化,伤口愈合,抗糖尿病和抗癌应用。
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-11-15 DOI: 10.1007/s12013-025-01949-2
Yasser M Taay, Mustafa Taha Mohammed, Ali Hussain Alwan, Ahmad Hussein Ismail
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引用次数: 0
In Vitro and In Vivo Studies of Skin Wound Healing Potential of Nanochitosan Grafted Curcumin and Lycopene in Wistar Albino Rats. 纳米壳聚糖移植姜黄素和番茄红素对Wistar白化大鼠皮肤创面愈合潜力的体外和体内研究。
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-11-12 DOI: 10.1007/s12013-025-01947-4
Sanjana Paddambail, Jayashree Sadasivam, Rangasamy Anandan, Pavan Kumar Dara, Sharadamma Narayanaswamy
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引用次数: 0
Therapeutic Potential of Phytocompounds Gentisic Acid and Alpha Resorcylic Acid against Alzheimer's Disease: A Network Pharmacology, In Silico, and In Vitro Approach. 植物化合物龙胆酸和间苯二甲酸对阿尔茨海默病的治疗潜力:网络药理学,计算机和体外方法。
IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-11-10 DOI: 10.1007/s12013-025-01944-7
Urvashi Soni, Rohini Pujari
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引用次数: 0
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Cell Biochemistry and Biophysics
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