BACKGROUNDDoxorubicin (DOX) has significant toxic side effects on cardiomyocytes, and existing preventive drug dexrazoxane has serious side effects. Therefore, in-depth research on drugs that can enhance the antitumor effect of DOX and simultaneously reduce its cardiotoxicity is of crucial significance. Our study explored the regulatory role of Erianin in DOX-induced cardiotoxicity and the specific molecular mechanism.METHODSIn this study, we constructed a myocardial injury model in mice with DOX. The toxic side effects of DOX on the organism were determined by recording the weight changes of the mice and calculating the spleen index and heart-tibia ratio of the mice. The degree of myocardial injury in mice was evaluated by methods such as echocardiography and Sirius red staining. Further in vivo experiments were conducted to verify whether the silencing of Nrf2 could block the protective effect of Erianin on myocardial cells.RESULTSWe found Erianin significantly alleviated DOX-induced cardiomyocyte injury (p < 0.0001), increased heart tissue pumping efficiency and contractility (p < 0.001), and reduced myocardial cell fibrosis. Mechanism study showed that Erianin can bind to Keap1, promote its ubiquitination and autophagic degradation, increase the acetylation of lysine 599 site in Nrf2 protein, and activate the antioxidant stress response.CONCLUSIONSTaken together, our study had for the first time elucidated the molecular mechanism by which Erianin alleviated DOX-induced myocardial injury by activating the Keap1-Nrf2 signaling pathway. It provides a theoretical basis for the development of Erianin as a potential protective drug for DOX-induced cardiotoxicity. It has very important clinical application and translational value.

2025-05-01·Inorganica Chimica Acta

Ruthenium(II) complexes synthesized as potential inducers of conformation inversion of AS1411 G4 DNA

作者: Deng, Wenhui ; Mei, Wenjie ; Liang, Jiangbo ; Huang, Peishan ; Hong, Wanwan ; Zhao, Bin ; Wu, Qiong ; Liu, Jing

Herein, four ruthenium(II) complexes, [Ru(L)2(PEIP)(CH2)4Br)](ClO4)2 (L = phen, 1; bpy, 2, PEIP = 2-(2-phenyl-ethenyl)-1H-imidazole-[4,5f][1,10]phenanthroline) and [Ru(L)2(PEIP)(CH2)4Erianin)](ClO4)2 (L = phen, 1E; bpy, 2E) have been synthesized and investigated as promising inducer to promote conformation inversion of AS1411 G4 DNA.All of these complexes can bind and stabilize AS1411 G4 DNA.Subsequent investigations reveal that in the presence of 1 and 1E, the described CD signal of AS1411 G4 DNA was reversed.Furthermore, it is discovered that in the presence of 1 and 1E, AS1411 G4 DNA can condense to a somewhat loose nano-network.Moreover, the anal. using mol. docking demonstrates that the conformation inversion of AS1411 G4 DNA is largely dependent on the binding sites of 1 and 1E.In conclusion, these complexes will be used for tumor diagnostics in the clin. context because of their capacity to stably bind AS1411 G4 DNA and dramatically boost its fluorescence emission.Besides, these complexes show promise as inducers of AS1411 G4 DNA conformational inversion.

2025-04-01·Environmental Toxicology

RETRACTION: Erianin Suppressed Lung Cancer Stemness and Chemotherapeutic Sensitivity via Triggering Ferroptosis

Article

RETRACTION: J. Lv, Z. Wang, and H. Liu, “Erianin Suppressed Lung Cancer Stemness and Chemotherapeutic Sensitivity via Triggering Ferroptosis,” Environmental Toxicology 39, no. 2 (2024): 479‐486, https://doi.org/10.1002/tox.23832.The above article, published online on 20 May 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.

项与 Erianin 相关的新闻（医药）

2023-03-22

·生物谷

双重靶向CRAF和MEK1/2为黑色素瘤和结肠癌症提供了一种有希望的治疗靶点

RAS-RAF-MEK-ERK信号传导级联（促分裂活化蛋白激酶途径）在调节细胞生长、分化和存活方面发挥着重要作用。然而，在许多携带RAS或RAF突变的肿瘤中，该途径经常被组成性激活。 RAS-RAF-MEK-ERK信号传导级联（促分裂活化蛋白激酶途径）在调节细胞生长、分化和存活方面发挥着重要作用。然而，在许多携带RAS或RAF突变的肿瘤中，该途径经常被组成性激活。据统计，KRAS突变发生在40%的结直肠癌和35%的非小细胞肺癌（NSCLC）中。此外，近20%的恶性黑色素瘤存在NRAS突变。RAF V600E突变发生在66%的皮肤黑色素瘤和25%的结直肠癌中。通常，没有B/CRAF激酶的空间激活和二聚化的BRAF V600E/K突变可以引起MAPK信号通路的持续组成型激活，而不依赖于RAS的启动。图片来源：https://doi.org/10.1038/s41392-023-01329-3 近日，来自郑州大学的研究者们在Signal Transduction and Targeted Therapy杂志上发表了题为“Erianin suppresses constitutive activation of MAPK signaling pathway by inhibition of CRAF and MEK1/2”的文章，该研究通过CRAF和MEK1/2的双重靶向性，为BRAF V600E或RAS突变黑色素瘤和结肠癌症提供了一种有希望的先导化合物。 RAS-RAF-MEK-ERK信号通路（MAPK通路）的组成性激活经常发生在许多携带RAS或RAF致癌突变的癌症中。由于单一使用BRAF或MEK抑制剂诱导的反常激活，双靶点RAF和MEK治疗被认为是一种有前途的策略。在这项工作中，研究者评估了erianin是一种新的CRAF和MEK1/2激酶抑制剂，从而抑制由BRAF V600E或RAS突变诱导的MAPK信号通路的组成型激活。KinaseProfiler酶谱分析、表面等离子体共振（SPR）、等温滴定量热法（ITC）、细胞热位移分析、计算对接和分子动力学模拟用于筛选和鉴定Eranin与CRAF和MEK1/2的结合。研究了激酶测定法、发光ADP检测法和酶动力学测定法，以确定MAPK在CRAF和MEK1/2激酶活性中的效率。值得注意的是，erinin通过抑制MEK1/2和CRAF而非BRAF激酶活性来抑制BRAF V600E或RAS突变黑色素瘤和结直肠癌细胞。此外，erinin在体内可减轻黑色素瘤和癌症。该模型描述了在BRAF V600E或RAS突变癌症中，MAPK蛋白抑制MAPK信号通路的组成型激活图片来源：https://doi.org/10.1038/s41392-023-01329-3 总之，erianin是CRAF和MEK1/2激酶的新型双重抑制剂，并抑制MAPK信号通路的组成型激活。基于这项研究，它在体内外显示了对各种BRAF V600E或KRAS突变癌症的活性，包括黑色素瘤和癌症。重要的是，本研究为黑色素瘤和结直肠癌的临床治疗提供了一种有前途的先导化合物，需要进一步的临床开发。（生物谷 Bioon.com）参考文献 Penglei Wang et al. Erianin suppresses constitutive activation of MAPK signaling pathway by inhibition of CRAF and MEK1/2. Signal Transduct Target Ther. 2023 Mar 6;8(1):96. doi: 10.1038/s41392-023-01329-3.