Baicalein, a component of banxia xiexin decoction, alleviates <scp>CPT</scp>‐11‐induced gastrointestinal dysfunction by inhibiting <scp>ALOX15</scp>‐mediated ferroptosis

Pei, Jingbo; Zou, Yuanyuan; Zhou, Wenying; Wang, Yakun

doi:10.1111/cbdd.14349

Cited by 3 publications

(1 citation statement)

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“…These tables serve as comprehensive up-to-date references, offering valuable insights into the diverse actions of polyphenols in modulating ferroptosis. [195] Decreases levels of ROS and ALOX15 / Cardiac arrest model in SD rats [196] Inhibits ferroptosis through a decrease in p53 acetylation level by elevating SIRT1…”

Section: Acute Lung Injury Treatment Through Ferroptosis Modulationmentioning

confidence: 99%

Beyond Mortality: Exploring the Influence of Plant Phenolics on Modulating Ferroptosis—A Systematic Review

Živanović,

Lesjak,

Simin

et al. 2024

Antioxidants

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Ferroptosis is a recently discovered type of programmed cell death that is mechanistically different from other types of programmed cell death such as apoptosis, necroptosis, and autophagy. It is characterized by the accumulation of intracellular iron, overproduction of reactive oxygen species, depletion of glutathione, and extensive lipid peroxidation of lipids in the cell membrane. It was discovered that ferroptosis is interconnected with many diseases, such as neurodegenerative diseases, ischemia/reperfusion injury, cancer, and chronic kidney disease. Polyphenols, plant secondary metabolites known for many bioactivities, are being extensively researched in the context of their influence on ferroptosis which resulted in a great number of publications showing the need for a systematic review. In this review, an extensive literature search was performed. Databases (Scopus, Web of Science, PubMed, ScienceDirect, Springer) were searched in the time span from 2017 to November 2023, using the keyword “ferroptosis” alone and in combination with “flavonoid”, “phenolic acid”, “stilbene”, “coumarin”, “anthraquinone”, and “chalcone”; after the selection of studies, we had 311 papers and 143 phenolic compounds. In total, 53 compounds showed the ability to induce ferroptosis, and 110 compounds were able to inhibit ferroptosis, and out of those compounds, 20 showed both abilities depending on the model system. The most researched compounds are shikonin, curcumin, quercetin, resveratrol, and baicalin. The most common modes of action are in the modulation of the Nrf2/GPX4 and Nrf2/HO-1 axis and the modulation of iron metabolism.

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Section: Acute Lung Injury Treatment Through Ferroptosis Modulationmentioning

confidence: 99%

Beyond Mortality: Exploring the Influence of Plant Phenolics on Modulating Ferroptosis—A Systematic Review

Živanović,

Lesjak,

Simin

et al. 2024

Antioxidants

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Ferroptosis: mechanisms and therapeutic targets

Zhou,

Meng,

et al. 2024

MedComm

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Ferroptosis is a nonapoptotic form of cell death characterized by iron‐dependent lipid peroxidation in membrane phospholipids. Since its identification in 2012, extensive research has unveiled its involvement in the pathophysiology of numerous diseases, including cancers, neurodegenerative disorders, organ injuries, infectious diseases, autoimmune conditions, metabolic disorders, and skin diseases. Oxidizable lipids, overload iron, and compromised antioxidant systems are known as critical prerequisites for driving overwhelming lipid peroxidation, ultimately leading to plasma membrane rupture and ferroptotic cell death. However, the precise regulatory networks governing ferroptosis and ferroptosis‐targeted therapy in these diseases remain largely undefined, hindering the development of pharmacological agonists and antagonists. In this review, we first elucidate core mechanisms of ferroptosis and summarize its epigenetic modifications (e.g., histone modifications, DNA methylation, noncoding RNAs, and N6‐methyladenosine modification) and nonepigenetic modifications (e.g., genetic mutations, transcriptional regulation, and posttranslational modifications). We then discuss the association between ferroptosis and disease pathogenesis and explore therapeutic approaches for targeting ferroptosis. We also introduce potential clinical monitoring strategies for ferroptosis. Finally, we put forward several unresolved issues in which progress is needed to better understand ferroptosis. We hope this review will offer promise for the clinical application of ferroptosis‐targeted therapies in the context of human health and disease.

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Targeting Hepatocellular Carcinoma: Schisandrin A Triggers Mitochondrial Disruption and Ferroptosis

He,

Lin,

Zhuang

et al. 2024

Chem Biol Drug Des

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The main focus of this research was to examine SchA's role in the hepatocellular carcinoma (HCC) development. LO2 and Huh7 cell viability were assessed using the MTT assay. The experiments included flow cytometry, colony formation, transwell, wound healing, and immunofluorescence assays to evaluate apoptosis levels, cells colony‐forming ability, ROS levels, invasion and migration ability, and mitochondrial membrane potential. Biochemical kits was utilized for checking the ATP, mitochondrial DNA, MDA, GSH, and Fe2+ levels in the Huh7 cells, and western blot for measuring the ferroptosis and AMPK/mTOR related‐protein expression levels. The MTT assay demonstrated that SchA significantly reduced the vitality of Huh7 cells ranging from 10 to 50 μM, whereas it exhibited no discernible impact on LO2 cells. Additionally, SchA significantly inhibited colony‐forming ability, invasion ability, and migration ability within the concentration range of 10 to 50 μM, with a reduction of 68% in colony formation at 50 μM. SchA also induced apoptosis in a dose‐dependent manner. Moreover, SchA was observed to significantly elevate ROS levels dose‐dependently, down‐regulate mitochondrial membrane potential (JC‐1) at 20 and 50 μM, and reduce the levels of ATP and mtDNA dose‐dependently. Various concentrations of SchA resulted in a notable elevation in MDA and Fe2+ levels as well as ACSL4 protein expression, accompanied by a reduction in GSH level and the protein expression of GPX4 and SLC7A11. Furthermore, SchA induced the activation of the AMPK/mTOR pathway in Huh7 cells, as evidenced by the increased phosphorylation level of AMPK and decreased phosphorylation level of mTOR. SchA might inhibit the progress of HCC through mitochondrial ferroptosis and dysfunction mediated by AMPK/mTOR pathway.

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Baicalein, a component of banxia xiexin decoction, alleviates CPT‐11‐induced gastrointestinal dysfunction by inhibiting ALOX15‐mediated ferroptosis

Cited by 3 publications

References 50 publications

Beyond Mortality: Exploring the Influence of Plant Phenolics on Modulating Ferroptosis—A Systematic Review

Beyond Mortality: Exploring the Influence of Plant Phenolics on Modulating Ferroptosis—A Systematic Review

Ferroptosis: mechanisms and therapeutic targets

Targeting Hepatocellular Carcinoma: Schisandrin A Triggers Mitochondrial Disruption and Ferroptosis

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