Paraquat-induced ferroptosis suppression via NRF2 expression regulation

Cai, Qiqi; Shen, Qingya; Zhu, Weimin; Zhang, Sheng; Ke, Jingjing; Lu, Zhongqiu

doi:10.1016/j.tiv.2023.105655

Toxicology in Vitro

2023

DOI: 10.1016/j.tiv.2023.105655

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Paraquat-induced ferroptosis suppression via NRF2 expression regulation

Qiqi Cai¹,

Qingya Shen²,

Weimin Zhu³

et al.

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2024

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Cited by 3 publications

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Mesenchymal stem cell-based therapy for paraquat-induced lung injury

Zhang,

Li,

2024

Cell Biol Toxicol

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Paraquat poisoning results in significant pulmonary damage, but current treatments are only minimally effective in repairing the injured lung tissues. Recent research has highlighted the promise of using stem cell therapy, namely mesenchymal stem cells, as a new method for treating paraquat toxicity. These cells have shown effectiveness in decreasing inflammation, apoptosis, and fibrosis in the mice lungs subjected to paraquat. The therapeutic implications of mesenchymal stem cells are believed to arise from their release of bioactive proteins and their capacity to regulate inflammatory responses. However, additional clinical study is required to validate these therapies' efficacy. This review thoroughly explores the pathophysiology of paraquat poisoning and the properties of mesenchymal stem cells. Additionally, it critically assesses the long-term safety and effectiveness of mesenchymal stem cell therapies, which is crucial for developing more dependable and effective treatment protocols. In summary, although mesenchymal stem cells offer promising prospects for treating lung injuries, more investigations are required to optimize their therapeutic promise and ensure their safe clinical application in the context of paraquat poisoning. Supplementary Information The online version contains supplementary material available at 10.1007/s10565-024-09911-3.

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Mesenchymal stem cell-based therapy for paraquat-induced lung injury

Zhang,

Li,

2024

Cell Biol Toxicol

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Inhibition of SLC40A1 represses osteoblast formation via inducing iron accumulation and activating the PERK/ATF4/CHOP pathway mediated oxidative stress

Fang,

Li,

Dong

et al. 2024

Redox Report

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Objective This study aimed to investigate the effects of solute carrier family 40 member 1 (SLC40A1) on iron accumulation, oxidative stress and differentiation in osteoblasts and potential mechanisms. Methods Mouse preosteoblastic MC3T3-E1 cells were transfected with the SLC40A1 overexpression vector (oeSLC40A1) and siRNA (siSLC40A1), then cell differentiation was induced via ascorbic acid and β-glycerophosphate. Besides, Ferrostatin-1 (ferroptosis inhibitor) and GSK2606414 (PERK inhibitor) were added with siSLC40A1. Results Fe 2+ , malondialdehyde (MDA), and reactive oxygen species (ROS) were higher but reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio was lower after siSLC40A1 transfection, while reduced Fe 2+ and ROS but elevated GSH/GSSG ratio was observed after oeSLC40A1 transfection. Alkaline phosphatase (ALP) staining, Alizarin Red S (ARS) staining, osteopontin (OPN) and bone morphogenetic protein 2 (BMP2) were lower after siSLC40A1 transfection but were greater after oeSLC40A1 transfection. Furthermore, SLC40A1 negatively regulated the PERK/ATF4/CHOP pathway. Further exploration revealed that Fe 2+ , MDA, ROS, and the PERK/ATF4/CHOP pathway were attenuated, while GSH/GSSG ratio, ALP staining, ARS staining, and OPN expression were increased after ferrostatin-1 treatment in the siSLC40A1-transfected cells. Similar trends were observed with respect to GSK2606414 treatment with siSLC40A1. Conclusion SLC40A1 inhibition suppresses osteoblast formation by facilitating iron accumulation and activating the PERK/ATF4/CHOP pathway-mediated oxidative stress.

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Decoding the power of saponins in ferroptosis regulation and disease intervention: a review

Ouyang,

Wu,

et al. 2024

Journal of Pharmacy and Pharmacology

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Objectives This review endeavors to elucidate the complex interplay underlying diseases associated with ferroptosis and to delineate the multifaceted mechanisms by which triterpenoid and steroidal saponins modulate this form of cell death. Methods A meticulous examination of the literature was undertaken, drawing from an array of databases including Web of Science, PubMed, and Wiley Library, with a focus on the keywords “ferroptosis,” “saponin,” “cancer,” “inflammation,” “natural products,” and “signaling pathways.” Key findings Ferroptosis represents a distinctive mode of cell death that holds considerable promise for the development of innovative therapeutic strategies targeting a wide range of diseases, especially cancer and inflammatory disorders. This review reveals the nuanced interactions between saponins and critical signaling pathways, including system Xc−-GSH-GPX4, Nrf2, p53, and mTOR. These interactions highlight the dual capacity of saponins to modulate ferroptosis, thereby offering fresh perspectives for therapeutic intervention. Conclusions The insights garnered from this review significantly advance our comprehension of the dynamic relationship between saponins and ferroptosis. By shedding light on these mechanisms, this work sets the stage for leveraging these insights in the creation of pioneering approaches to disease treatment, marking a significant stride in the evolution of therapeutic modalities.

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Paraquat-induced ferroptosis suppression via NRF2 expression regulation

Cited by 3 publications

References 31 publications

Mesenchymal stem cell-based therapy for paraquat-induced lung injury

Mesenchymal stem cell-based therapy for paraquat-induced lung injury

Inhibition of SLC40A1 represses osteoblast formation via inducing iron accumulation and activating the PERK/ATF4/CHOP pathway mediated oxidative stress

Decoding the power of saponins in ferroptosis regulation and disease intervention: a review

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