Rehmannioside A improves cognitive impairment and alleviates ferroptosis via activating PI3K/AKT/Nrf2 and SLC7A11/GPX4 signaling pathway after ischemia

Journal of Ethnopharmacology, Год журнала: 2022, Номер 289, С. 115021 - 115021

Опубликована: Янв. 26, 2022

Язык: Английский

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Targeting ferroptosis in acute kidney injury

Cell Death and Disease, Год журнала: 2022, Номер 13(2)

Опубликована: Фев. 24, 2022

Acute kidney injury (AKI) is a major public health problem with high incidence and mortality. As form of programmed cell death (PCD), ferroptosis could be considered as process iron accumulation enhanced lipid peroxidation. Recently, the fundamental roles in AKI have attracted much attention. The network mechanism its to chronic disease (CKD) transition complicated multifactorial. Strategies targeting show great potential. Here, we review research progress on participation AKI. We hope that this work will provide clues for further studies

Язык: Английский

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Cell Death Mechanisms in Cerebral Ischemia–Reperfusion Injury

Neurochemical Research, Год журнала: 2022, Номер 47(12), С. 3525 - 3542

Опубликована: Авг. 17, 2022

Язык: Английский

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Empagliflozin attenuates the renal tubular ferroptosis in diabetic kidney disease through AMPK/NRF2 pathway

Free Radical Biology and Medicine, Год журнала: 2022, Номер 195, С. 89 - 102

Опубликована: Дек. 27, 2022

Язык: Английский

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Quercetin alleviates kainic acid-induced seizure by inhibiting the Nrf2-mediated ferroptosis pathway

Free Radical Biology and Medicine, Год журнала: 2022, Номер 191, С. 212 - 226

Опубликована: Сен. 7, 2022

Epilepsy is one of the most common neurological disorders in childhood. However, classical antiepileptic drugs are linked with drug toxicity and cognitive function impairment children. Hence, it essential to develop a novel therapy solve this problem. Currently, studies indicate regulating nuclear factor-erythroid 2-related factor 2 (Nrf2)-mediated ferroptosis pathway represents potential advanced for seizures. present study aimed explore whether quercetin, natural polyphenol, could alleviate seizure-induced neuron death preserve by inhibiting Nrf2-mediated ferroptosis.Kainic acid-induced epileptic mice model, morris water maze (MWM) test, cell counting kit-8 (CCK-8) assays, western blotting analysis, enzyme-linked immunosorbent assay, flow cytometry, quantitative real-time reverse transcription PCR (qRT-PCR), immunofluorescence staining, RNA sequencing analysis were employed mechanisms which quercetin exerts protective effects on kainic model glutamate-induced HT22 neuronal death.Our findings suggested association between seizures clinical setting. Quercetin pretreatment alleviates seizure-like behaviors KA-induced mice. Additionally, vitro, co-treatment effectively neuroprotective death. These also closely pathway. Furthermore, bioinformatic profiling revealed that SIRT1/Nrf2/SLC7A11/GPX4 plays crucial role Glu-induced pretreated quercetin.These indicated protects against vivo vitro via

Язык: Английский

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High Level of Uric Acid Promotes Atherosclerosis by Targeting NRF2-Mediated Autophagy Dysfunction and Ferroptosis

Oxidative Medicine and Cellular Longevity, Год журнала: 2022, Номер 2022, С. 1 - 21

Опубликована: Апрель 18, 2022

Atherosclerotic vascular disease (ASVD) is the leading cause of death worldwide. Hyperuricemia fourth risk factor for atherosclerosis after hypertension, diabetes, and hyperlipidemia. The mechanism hyperuricemia affecting occurrence development has not been fully elucidated. Mononuclear macrophages play critical roles in all stages atherosclerosis. Studies have confirmed that both ferroptosis promote atherosclerosis, but whether high level uric acid (HUA) promotes by regulating remains unclear. We found HUA significantly promoted atherosclerotic plaque downregulated protein NRF2/SLC7A11/GPX4 signaling pathway ApoE-/- mice. Next, we evaluated effect inhibitor ferrostatin-1 (Fer-1) treatment on formation macrophage-derived foam cells. cells, decreased cell viability, increased iron accumulation lipid peroxidation treated with oxidized low-density lipoprotein (oxLDL); these effects were reversed Fer-1 treatment. Mechanistically, inhibited autophagy pathway. activated upregulated ferroptosis-associated proteins. Moreover, an NRF2 inducer (tertbutyl hydroquinone (TBHQ)) activator (rapamycin (RAPA)) could reverse inhibitory survival. Our results suggest HUA-induced involved plaques. More importantly, enhancing inhibiting activating may alleviate These findings might contribute to a deeper understanding role pathogenesis provide therapeutic target ASVD associated hyperuricemia.

Язык: Английский

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Lentinan inhibits oxidative stress and alleviates LPS-induced inflammation and apoptosis of BMECs by activating the Nrf2 signaling pathway

International Journal of Biological Macromolecules, Год журнала: 2022, Номер 222, С. 2375 - 2391

Опубликована: Окт. 13, 2022

Язык: Английский

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The mechanism of microglia-mediated immune inflammation in ischemic stroke and the role of natural botanical components in regulating microglia: A review

Frontiers in Immunology, Год журнала: 2023, Номер 13

Опубликована: Фев. 2, 2023

Ischemic stroke (IS) is one of the most fatal diseases. Neuroimmunity, inflammation, and oxidative stress play important roles in various complex mechanisms IS. In particular, early proinflammatory response resulting from overactivation resident microglia infiltration circulating monocytes macrophages brain after cerebral ischemia leads to secondary injury. Microglia are innate immune cells that constantly monitor microenvironment under normal conditions. Once occurs, activated produce dual effects neurotoxicity neuroprotection, balance two determines fate damaged neurons. The activation defined as classical (M1 type) or alternative (M2 type). M1 type secrete pro-inflammatory cytokines neurotoxic mediators exacerbate neuronal damage, while M2 promote a repairing anti-inflammatory response. Fine regulation M1/M2 microglial minimize damage maximize protection has therapeutic value. This review focuses on interaction between other involved IS phenotypic characteristics, mechanism natural plant components regulating IS, providing novel candidate drugs for drug development.

Язык: Английский

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The mechanism of ferroptosis and its related diseases

Molecular Biomedicine, Год журнала: 2023, Номер 4(1)

Опубликована: Окт. 16, 2023

Abstract Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation lipid peroxides, provides novel avenue for delving into intersection metabolism, oxidative stress, and disease pathology. We have witnessed mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, traumatic tissue injuries. By unraveling intricate underpinnings molecular machinery, contributors, signaling conduits, regulatory networks governing researchers aim bridge gap between intricacies this unique mode multifaceted implications health disease. In light rapidly advancing landscape ferroptosis research, we present comprehensive review aiming at extensive in origins progress human diseases. This concludes careful analysis potential treatment approaches carefully designed either inhibit or promote ferroptosis. Additionally, succinctly summarized therapeutic targets compounds that hold promise targeting within various facet underscores burgeoning possibilities manipulating as strategy. summary, enriched insights both investigators practitioners, while fostering an elevated comprehension latent translational utilities. revealing basic processes investigating possibilities, crucial resource scientists medical aiding deep understanding effects situations.

Язык: Английский

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Mitochondrial dysfunctions induce PANoptosis and ferroptosis in cerebral ischemia/reperfusion injury: from pathology to therapeutic potential

Frontiers in Cellular Neuroscience, Год журнала: 2023, Номер 17

Опубликована: Май 24, 2023

Ischemic stroke (IS) accounts for more than 80% of the total stroke, which represents leading cause mortality and disability worldwide. Cerebral ischemia/reperfusion injury (CI/RI) is a cascade pathophysiological events following restoration blood flow reoxygenation, not only directly damages brain tissue, but also enhances series pathological signaling cascades, contributing to inflammation, further aggravate damage tissue. Paradoxically, there are still no effective methods prevent CI/RI, since detailed underlying mechanisms remain vague. Mitochondrial dysfunctions, characterized by mitochondrial oxidative stress, Ca 2+ overload, iron dyshomeostasis, DNA (mtDNA) defects quality control (MQC) disruption, closely relevant process CI/RI. There increasing evidence that dysfunctions play vital roles in regulation programmed cell deaths (PCDs) such as ferroptosis PANoptosis, newly proposed conception unique form innate immune inflammatory death regulated multifaceted PANoptosome complexes. In present review, we highlight how this key event contributes response well modes during Neuroprotective agents targeting may serve promising treatment strategy alleviate serious secondary injuries. A comprehensive insight into dysfunctions-mediated PCDs can help provide strategies guide therapies CI/RI IS.

Язык: Английский

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