Jiedu Huayu Extract Alleviate Acute Liver Failure via Promotion of GPX4 Expression and Inhibition of D-GalN/LPS-Induced Ferroptosis DOI Creative Commons
Yong Lin, Yong Du, Minggang Wang

et al.

Natural Product Communications, Journal Year: 2024, Volume and Issue: 19(12)

Published: Dec. 1, 2024

Objective This study aims to explore the potential mechanisms of Jiedu Huayu granules (JDHY) mitigate D-galactosamine (D-GalN) and lipopolysaccharide (LPS)-induced acute liver failure (ALF) in a cell damage model. Methods ALF was modeled using various concentrations D-GalN + LPS. JDHY-medicated serum at different then co-cultured with model proportion. The best concentration time intervention were determined by Cell Counting Kit-8, Alanine Aminotransferase (ALT), Aspartate (AST). Western blot used assess expression Ferritin Heavy Chain 1 (FTH1), Transferrin Receptor 1(TfR1), Glutathione Peroxidase 4 (GPX4), Lysyl Oxidase (LOX), Prostaglandin-Endoperoxide Synthase 2(PTGS2). Malondialdehyde analyzed for lipid peroxidation, enzyme-linked immunosorbent assay detect glutathione, Tumor Necrosis Factor-alpha, Interleukin-10, Interleukin-6 expression, function indicators (ALT, AST). Additionally, GPX4 knocked down transfection, molecular JDHY treating explored through blot, PCR, assay. Results appropriate dose D-GalN/LPS-induced (10 mg/mL μg/mL LPS 48 h) optimal (15%) ALT, AST, Kit-8 assays. treatment reduced ALT AST levels, alleviated inhibited ferroptosis. mechanism involves enhancing antioxidant capacity cells increasing regulating ferroptosis proteins (downregulating TfR1, upregulating FTH1), inhibiting LOX PTGS2, suppressing inflammation Factor-alpha Interleukin-6, Interleukin-10). In addition, knockdown experiments revealed that knocking worsened ALF, while can alleviate promoting cells. Conclusion enhance reduce peroxidation affected protecting cell, alleviating inflammatory,

Language: Английский

A new strategy for the treatment of intracerebral hemorrhage: Ferroptosis DOI

Ke Yao Sun,

Xin Yue Bai,

Lei Zhang

et al.

Experimental Neurology, Journal Year: 2024, Volume and Issue: 382, P. 114961 - 114961

Published: Sept. 15, 2024

Language: Английский

Citations

2
Ferroptosis in hepatocellular carcinoma: Mechanisms and therapeutic implications DOI Open Access

Shanjie Tu,

Yisheng Zou,

Meiqi Yang

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 182, P. 117769 - 117769

Published: Dec. 16, 2024

Language: Английский

Citations

2
Mechanisms of Vitamins Inhibiting Ferroptosis DOI Creative Commons
Meng Zhang, Xin Chen,

Yumei Zhang

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(12), P. 1571 - 1571

Published: Dec. 20, 2024

Ferroptosis is an iron-dependent form of cell death, which characterized by the uncontrolled and overwhelming peroxidation membrane lipids. has been implicated in progression various pathologies, including steatotic liver, heart failure, neurodegenerative diseases, diabetes. Targeted inhibition ferroptosis provides a promising strategy to treat ferroptosis-related diseases. Multivitamins, vitamins A, B, C, D, E, K, have shown good ability inhibit ferroptosis. For example, vitamin A significantly upregulated expression several key ferroptotic gatekeepers genes through nuclear retinoic acid receptors X (RAR/RXR). Vitamin B6 could compensate for impaired glutathione (GSH) levels restore Glutathione peroxidase 4 (GPX4) cells, ultimately inhibiting D up-regulate anti-ferroptosis proteins activating receptors. E hydroquinone K (VKH2) can directly propagation lipid peroxidation, thereby In this review, we summarize currently understood mechanisms provide reference information future research on development inhibitors.

Language: Английский

Citations

1
Design and Synthesis of 1,4‐Diformyl‐Piperazine Ferrostatin‐1 Derivatives as Novel Ferroptosis Inhibitors DOI Open Access
Yifan Zhang, Wei Guo, Hui Zheng

et al.

Chemical Biology & Drug Design, Journal Year: 2024, Volume and Issue: 104(5)

Published: Oct. 28, 2024

ABSTRACT The present study focuses on the design and synthesis of novel 1,4‐diformyl‐piperazine‐based ferrostatin‐1 (Fer‐1) derivatives, their evaluation against ferroptosis activity. synthesized compounds demonstrated significant anti‐ferroptosis activity in human umbilical vascular endothelial cells (HUVECs), with Compound 24 showing highest potency. Mechanistic studies revealed that effectively reduced intracellular reactive oxygen species (ROS) levels, mitigated mitochondrial damage, enhanced glutathione peroxidase 4 (GPX4) expression. Additionally, exhibited improved solubility plasma stability compared to control compounds, Fer‐1 JHL‐12. These findings suggest derivatives hold promise as therapeutic agents for ferroptosis‐associated cardiovascular diseases.

Language: Английский

Citations

0
Discovery of phenazine derivatives as a new class of non-classical ferroptosis inhibitors and efficacy evaluation on a mouse model of liver injury DOI
Yunjie Wu, Yang Lu, Jing You

et al.

European Journal of Medicinal Chemistry, Journal Year: 2024, Volume and Issue: 282, P. 117042 - 117042

Published: Nov. 12, 2024

Language: Английский

Citations

0
[Ferroptosis inducer Erastin inhibits proliferation of liver cancer cells DOI
Pan Zhao, Zihui Zhou, Liang Yu

et al.

PubMed, Journal Year: 2024, Volume and Issue: 44(11), P. 2131 - 2136

Published: Nov. 20, 2024

To investigate the expression of Acyl-CoA synthetase long-chain family member 4 (ACSL4) in liver cancer and its role regulating ferroptosis proliferation cells.

Language: Английский

Citations

0
Jiedu Huayu Extract Alleviate Acute Liver Failure via Promotion of GPX4 Expression and Inhibition of D-GalN/LPS-Induced Ferroptosis DOI Creative Commons
Yong Lin, Yong Du, Minggang Wang

et al.

Natural Product Communications, Journal Year: 2024, Volume and Issue: 19(12)

Published: Dec. 1, 2024

Objective This study aims to explore the potential mechanisms of Jiedu Huayu granules (JDHY) mitigate D-galactosamine (D-GalN) and lipopolysaccharide (LPS)-induced acute liver failure (ALF) in a cell damage model. Methods ALF was modeled using various concentrations D-GalN + LPS. JDHY-medicated serum at different then co-cultured with model proportion. The best concentration time intervention were determined by Cell Counting Kit-8, Alanine Aminotransferase (ALT), Aspartate (AST). Western blot used assess expression Ferritin Heavy Chain 1 (FTH1), Transferrin Receptor 1(TfR1), Glutathione Peroxidase 4 (GPX4), Lysyl Oxidase (LOX), Prostaglandin-Endoperoxide Synthase 2(PTGS2). Malondialdehyde analyzed for lipid peroxidation, enzyme-linked immunosorbent assay detect glutathione, Tumor Necrosis Factor-alpha, Interleukin-10, Interleukin-6 expression, function indicators (ALT, AST). Additionally, GPX4 knocked down transfection, molecular JDHY treating explored through blot, PCR, assay. Results appropriate dose D-GalN/LPS-induced (10 mg/mL μg/mL LPS 48 h) optimal (15%) ALT, AST, Kit-8 assays. treatment reduced ALT AST levels, alleviated inhibited ferroptosis. mechanism involves enhancing antioxidant capacity cells increasing regulating ferroptosis proteins (downregulating TfR1, upregulating FTH1), inhibiting LOX PTGS2, suppressing inflammation Factor-alpha Interleukin-6, Interleukin-10). In addition, knockdown experiments revealed that knocking worsened ALF, while can alleviate promoting cells. Conclusion enhance reduce peroxidation affected protecting cell, alleviating inflammatory,

Language: Английский

Citations

0