Propofol Inhibits Ferroptotic Cell Death Through the Nrf2/Gpx4 Signaling Pathway in the Mouse Model of Cerebral Ischemia–Reperfusion Injury

Fan, Gui-Bo; Li, Yan; Xu, Gao-Shuo; Zhao, A-Yang; Jin, Hong-Jiang; Sun, Shuliang; Qi, Shijie

doi:10.1007/s11064-022-03822-7

Cited by 13 publications

(10 citation statements)

References 52 publications

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“…105 Also, due to its potent antioxidant properties, propofol protected against cerebral ischemia reperfusion injury (CIRI) induced ferroptosis via Nrf2/Gpx4 signaling. 106 In addition, propofol inhibited ischemia/reperfusion (I/R)-induced ferroptosis in neurons by inhibiting the HIF-1α/YTHDF1/BECN1 axis. 107 In contrast to these studies, repeated propofol anesthesia (continuous 200 mg/kg) promoted hippocampal ferroptosis and cognitive dysfunction in aging rats.…”

Section: Iron Homeos Ta S Is Ferrop Tos Is and Other G Ener Al Ane ...mentioning

confidence: 99%

“…In HT‐22 cells, propofol (50 μM) downregulated erastin‐induced iron accumulation, excess ROS, and lipid peroxidation by upregulating system Xc‐ and GPX4 105 . Also, due to its potent antioxidant properties, propofol protected against cerebral ischemia reperfusion injury (CIRI) induced ferroptosis via Nrf2/Gpx4 signaling 106 . In addition, propofol inhibited ischemia/reperfusion (I/R)‐induced ferroptosis in neurons by inhibiting the HIF‐1α/YTHDF1/BECN1 axis 107 .…”

Section: Iron Homeostasis Ferroptosis and Other General Anestheticsmentioning

confidence: 99%

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Dysregulation of iron homeostasis and ferroptosis in sevoflurane and isoflurane associated perioperative neurocognitive disorders

Miao,

Han,

Wang

et al. 2024

CNS Neurosci Ther

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In recent years, sevoflurane and isoflurane are the most popular anesthetics in general anesthesia for their safe, rapid onset, and well tolerant. Nevertheless, many studies reported their neurotoxicity among pediatric and aged populations. This effect is usually manifested as cognitive impairment such as perioperative neurocognitive disorders. The wide application of sevoflurane and isoflurane during general anesthesia makes their safety a major health concern. Evidence indicates that iron dyshomeostasis and ferroptosis may establish a role in neurotoxicity of sevoflurane and isoflurane. However, the mechanisms of sevoflurane‐ and isoflurane‐induced neuronal injury were not fully understood, which poses a barrier to the treatment of its neurotoxicity. We, therefore, reviewed the current knowledge on mechanisms of iron dyshomeostasis and ferroptosis and aimed to promote a better understanding of their roles in sevoflurane‐ and isoflurane‐induced neurotoxicity.

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Section: Iron Homeos Ta S Is Ferrop Tos Is and Other G Ener Al Ane ...mentioning

confidence: 99%

Section: Iron Homeostasis Ferroptosis and Other General Anestheticsmentioning

confidence: 99%

Dysregulation of iron homeostasis and ferroptosis in sevoflurane and isoflurane associated perioperative neurocognitive disorders

Miao,

Han,

Wang

et al. 2024

CNS Neurosci Ther

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“…A more direct role of Nrf2 in neuroprotection is through mitigating oxidative stress by clearance of ROS, and alleviating excitotoxic injury which has been thoroughly reviewed elsewhere. 46 Sublethal excitotoxicity in the penumbra predominantly leads to apoptosis rather than necrosis. It is worth noting that many studies only proved the association without further elucidating the causality.…”

Section: Cell‐specific Role Of Nrf2 In the Acute Phasementioning

confidence: 99%

“… 64 , 65 Therefore, Nrf2 could be a major regulator of lipid peroxidation and ferroptosis. 66 Indeed, Nrf2 is critical for the anti‐ferroptotic effects of neuroprotective compounds such as vitexin, 67 elabela, 68 and inhaled propofol, 46 and miRNA‐27a directly binds to the Nrf2 gene, inhibiting its expression which exacerbates ferroptosis. 68 A limitation of ferroptosis research is that GSS and GPX4 are typically applied as markers for ferroptosis, but the potential involvement of other types of cell death has not been evaluated.…”

Section: Cell‐specific Role Of Nrf2 In the Acute Phasementioning

confidence: 99%

The cell‐specific roles of Nrf2 in acute and chronic phases of ischemic stroke

Fadoul,

Ikonomovic,

Zhang

et al. 2023

CNS Neurosci Ther

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Ischemic stroke refers to the sudden loss of blood flow in a specific area of the brain. It is the fifth leading cause of mortality and the leading cause of permanent disability. The transcription factor nuclear factor erythroid 2‐related factor 2 (Nrf2) controls the production of several antioxidants and protective proteins and it has been investigated as a possible pharmaceutical target for reducing harmful oxidative events in brain ischemia. Each cell type exhibits different roles and behaviors in different phases post‐stroke, which is comprehensive yet important to understand to optimize management strategies and goals for care for stroke patients. In this review, we comprehensively summarize the protective effects of Nrf2 in experimental ischemic stroke, emphasizing the role of Nrf2 in different cell types including neurons, astrocytes, oligodendrocytes, microglia, and endothelial cells during acute and chronic phases of stroke and providing insights on the neuroprotective role of Nrf2 on each cell type throughout the long term of stroke care. We also highlight the importance of targeting Nrf2 in clinical settings while considering a variety of important factors such as age, drug dosage, delivery route, and time of administration.

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“…This is because in basic experiments, we often use holding devices to ensure that the body temperature of the animals is constant and to prevent the neuroprotective effects of hypothermia from interfering with the experiment. In the context of temperature control, there are still basic research studies that confirm the neuroprotective effect of propofol ( Fan et al, 2022 ).…”

Section: The Neuroprotective Properties Of Some Anesthetic Drugs In B...mentioning

confidence: 99%

A retrospect and outlook on the neuroprotective effects of anesthetics in the era of endovascular therapy

et al. 2023

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Studies on the neuroprotective effects of anesthetics were carried out more than half a century ago. Subsequently, many cell and animal experiments attempted to verify the findings. However, in clinical trials, the neuroprotective effects of anesthetics were not observed. These contradictory results suggest a mismatch between basic research and clinical trials. The Stroke Therapy Academic Industry Roundtable X (STAIR) proposed that the emergence of endovascular thrombectomy (EVT) would provide a proper platform to verify the neuroprotective effects of anesthetics because the haemodynamics of patients undergoing EVT is very close to the ischaemia–reperfusion model in basic research. With the widespread use of EVT, it is necessary for us to re-examine the neuroprotective effects of anesthetics to guide the use of anesthetics during EVT because the choice of anesthesia is still based on team experience without definite guidelines. In this paper, we describe the research status of anesthesia in EVT and summarize the neuroprotective mechanisms of some anesthetics. Then, we focus on the contradictory results between clinical trials and basic research and discuss the causes. Finally, we provide an outlook on the neuroprotective effects of anesthetics in the era of endovascular therapy.

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Propofol Inhibits Ferroptotic Cell Death Through the Nrf2/Gpx4 Signaling Pathway in the Mouse Model of Cerebral Ischemia–Reperfusion Injury

Cited by 13 publications

References 52 publications

Dysregulation of iron homeostasis and ferroptosis in sevoflurane and isoflurane associated perioperative neurocognitive disorders

Dysregulation of iron homeostasis and ferroptosis in sevoflurane and isoflurane associated perioperative neurocognitive disorders

The cell‐specific roles of Nrf2 in acute and chronic phases of ischemic stroke

A retrospect and outlook on the neuroprotective effects of anesthetics in the era of endovascular therapy

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