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Isoliensinine activated the Nrf2/GPX4 pathway to inhibit glutamate-induced ferroptosis in HT-22 cells.

التفاصيل البيبلوغرافية
العنوان: Isoliensinine activated the Nrf2/GPX4 pathway to inhibit glutamate-induced ferroptosis in HT-22 cells.
المؤلفون: Long HZ; Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.; Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, School of Pharmacy of University of South China, Hengyang, China., Li FJ; Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.; Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, School of Pharmacy of University of South China, Hengyang, China., Gao LC; Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.; Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, School of Pharmacy of University of South China, Hengyang, China., Zhou ZW; Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.; Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, School of Pharmacy of University of South China, Hengyang, China., Luo HY; Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.; Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, School of Pharmacy of University of South China, Hengyang, China., Xu SG; Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.; Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, School of Pharmacy of University of South China, Hengyang, China., Dai SM; Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.; Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, School of Pharmacy of University of South China, Hengyang, China., Hu JD; Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.; Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, School of Pharmacy of University of South China, Hengyang, China.
المصدر: Journal of biochemical and molecular toxicology [J Biochem Mol Toxicol] 2024 Sep; Vol. 38 (9), pp. e23794.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Wiley Country of Publication: United States NLM ID: 9717231 Publication Model: Print Cited Medium: Internet ISSN: 1099-0461 (Electronic) Linking ISSN: 10956670 NLM ISO Abbreviation: J Biochem Mol Toxicol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: New York, NY : Wiley, c1998-
مواضيع طبية MeSH: Ferroptosis*/drug effects , Glutamic Acid*/toxicity , Glutamic Acid*/metabolism , Phospholipid Hydroperoxide Glutathione Peroxidase*/metabolism , NF-E2-Related Factor 2*/metabolism , Signal Transduction*/drug effects, Animals ; Mice ; Cell Line ; Isoquinolines/pharmacology ; Neurons/drug effects ; Neurons/metabolism
مستخلص: Isoliensinine (ISO), a natural compound, is a bibenzyl isoquinoline alkaloid monomer in lotus seed, which has strong antioxidant and free radical scavenging activities. The oxidative toxicity caused by glutamic acid overdose is one of the important mechanisms of nerve cell injury, and the oxidative toxicity caused by glutamic acid is related to ferroptosis. This study aims to establish a glutamate-induced injury model of mouse hippocampal neurons HT-22 cells, and investigate the protective effect of ISO on the neurotoxicity of glutamate-induced HT-22 cells. The results showed that ISO inhibited glutamate-induced ferroptosis of neuronal cells through nuclear factor E2-related factor 2/glutathione peroxidase 4 (Nrf2/GPX4) signaling pathway. Pretreatment of HT-22 cells with ISO significantly reduced glutamate-induced cell death. Ferroptosis inhibitors have the same effect. ISO inhibited the decrease of mitochondrial membrane potential detection and the increase of iron content induced by glutamate, the increase of malondialdehyde and reactive oxygen species in cytoplasm and lipid, and protected the activities of GPx and superoxide dismutase enzymes. In addition, WB showed that glutamic acid could induce the upregulated expression of long-chain esteryl coA synthase 4 (ACSL4) protein and the downregulated expression of SLC7A11 and GPX4 protein in HT-22 cells, while ISO could prevent the abnormal expression of these proteins induced by glutamic acid. The nuclear translocation of Nrf2 in HT-22 cells was increased, and the expression of downstream heme oxygenase-1 protein was upregulated. In summary, ISO protects HT-22 cells from glutamate-induced ferroptosis through a novel mechanism of the Nrf2/GPX4 signaling pathway.
(© 2024 Wiley Periodicals LLC.)
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معلومات مُعتمدة: 2021JJ30753 Natural Science Foundation of Hunan Province; Hunan Provincial Health High-level Talents Support Program; 22A0320 Scientific research Project of education department of Hunan province; YNKY202205 Changsha Central Hospital Affiliated to University of South China Foundation of key Program
فهرسة مساهمة: Keywords: Nrf2/GPX4 pathway; ferroptosis; glutamate; isoliensinine; neurodegenerative diseases
المشرفين على المادة: 3KX376GY7L (Glutamic Acid)
EC 1.11.1.12 (Phospholipid Hydroperoxide Glutathione Peroxidase)
0 (NF-E2-Related Factor 2)
0 (Nfe2l2 protein, mouse)
EC 1.11.1.9 (glutathione peroxidase 4, mouse)
0 (Isoquinolines)
تواريخ الأحداث: Date Created: 20240820 Date Completed: 20240820 Latest Revision: 20240820
رمز التحديث: 20240821
DOI: 10.1002/jbt.23794
PMID: 39163615
قاعدة البيانات: MEDLINE
الوصف
تدمد:1099-0461
DOI:10.1002/jbt.23794