We are analyzing https://link.springer.com/article/10.1007/s11064-022-03822-7.

Title:
Propofol Inhibits Ferroptotic Cell Death Through the Nrf2/Gpx4 Signaling Pathway in the Mouse Model of Cerebral Ischemia–Reperfusion Injury | Neurochemical Research
Description:
Ferroptosis is characterized by excessive accumulation of iron and lipid peroxides, which are involved in ischemia, reperfusion-induced organ injury, and stroke. Propofol, an anesthetic agent, has neuroprotective effects due to its potent antioxidant, anti-ischemic, and anti-inflammatory properties. However, the relationship between propofol and ferroptosis is still unclear. In the current study, we elucidated the role of ferroptosis in the neuroprotective effect of propofol in mouse brains subjected to cerebral ischemia reperfusion injury (CIRI). Ferroptosis was confirmed by Western blotting assays, transmission electron microscopy, and glutathione assays. Propofol regulated Nrf2/Gpx4 signaling, enhanced antioxidant potential, inhibited the accumulation of lipid peroxides in CIRI-affected neurons, and significantly reversed CIRI-induced ferroptosis. Additionally, Gpx4 inhibitor RSL3 and Nrf2 inhibitor ML385 attenuated the effects of propofol on antioxidant capacity, lipid peroxidation, and ferroptosis in CIRI-affected neurons. Our data support a protective role of propofol against ferroptosis as a cause of cell death in mice with CIRI. Propofol protected against CIRI-induced ferroptosis partly by regulating the Nrf2/Gpx4 signaling pathway. These findings may contribute to the development of future therapies targeting ferroptosis induced by CIRI.
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Keywords {🔍}

pubmed, article, google, scholar, cas, ferroptosis, cell, central, propofol, death, injury, zhang, wang, pathway, signaling, liu, ischemiareperfusion, brain, cerebral, zhao, nrf, res, chen, data, stroke, httpsdoiorgs, httpsdoiorg, cancer, research, nrfgpx, fan, neurons, oxidative, ischemic, model, lipid, regulating, authors, privacy, cookies, content, mouse, manuscript, sun, gpx, attenuates, stress, activation, mol, rats,

Topics {✒️}

nf-kappab/hif-1alpha signaling hypoxia-ischemia-induced brain injury akt/nrf2/gpx4 signaling pathway month download article/chapter cerebral ischemia–reperfusion injury reperfusion-induced organ injury myocardial ischemia-reperfusion injury si-hua qi nrf2/gpx4 signaling pathway nrf2/nlrp3 signaling pathway pi3k/akt-mptp pathway ferroptosis-mediated tissue injury facilitating chaperone-mediated autophagy gpx4 inhibitor-induced ferroptosis ppargamma/hmgb1/nlrp3 axis nrf2 signaling pathway ciri-induced ferroptosis partly nrf2/gpx4 pathway focal cerebral ischemia full article pdf intestinal ischemia/reperfusion prevent redundant research renal cell cancer related subjects iron-dependent form clear-cell morphology selenium inhibits ferroptosis privacy choices/manage cookies gpx4 inhibitor rsl3 dixon sj sesamin attenuates neurotoxicity yang ws stockwell br inhibiting oxidative stress ischemic brain stroke reprogramming glycogen metabolism nonapoptotic cell death gallbladder cancer cells propofol induces proliferation apoptosis entosis mechanism fumarate hydratase inactivation vascular endothelial cells facilitating 4-hne clearance ischemia-reperfusion regulating iron homeostasis holds exclusive rights mitigating lipid peroxidation article fan european economic area transmission electron microscopy

Questions {❓}

Van der Kooij MA, Groenendaal F, Kavelaars A, Heijnen CJ, van Bel F (2009) Combination of deferoxamine and erythropoietin: therapy for hypoxia-ischemia-induced brain injury in the neonatal rat?

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         description:Ferroptosis is characterized by excessive accumulation of iron and lipid peroxides, which are involved in ischemia, reperfusion-induced organ injury, and stroke. Propofol, an anesthetic agent, has neuroprotective effects due to its potent antioxidant, anti-ischemic, and anti-inflammatory properties. However, the relationship between propofol and ferroptosis is still unclear. In the current study, we elucidated the role of ferroptosis in the neuroprotective effect of propofol in mouse brains subjected to cerebral ischemia reperfusion injury (CIRI). Ferroptosis was confirmed by Western blotting assays, transmission electron microscopy, and glutathione assays. Propofol regulated Nrf2/Gpx4 signaling, enhanced antioxidant potential, inhibited the accumulation of lipid peroxides in CIRI-affected neurons, and significantly reversed CIRI-induced ferroptosis. Additionally, Gpx4 inhibitor RSL3 and Nrf2 inhibitor ML385 attenuated the effects of propofol on antioxidant capacity, lipid peroxidation, and ferroptosis in CIRI-affected neurons. Our data support a protective role of propofol against ferroptosis as a cause of cell death in mice with CIRI. Propofol protected against CIRI-induced ferroptosis partly by regulating the Nrf2/Gpx4 signaling pathway. These findings may contribute to the development of future therapies targeting ferroptosis induced by CIRI.
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      description:Ferroptosis is characterized by excessive accumulation of iron and lipid peroxides, which are involved in ischemia, reperfusion-induced organ injury, and stroke. Propofol, an anesthetic agent, has neuroprotective effects due to its potent antioxidant, anti-ischemic, and anti-inflammatory properties. However, the relationship between propofol and ferroptosis is still unclear. In the current study, we elucidated the role of ferroptosis in the neuroprotective effect of propofol in mouse brains subjected to cerebral ischemia reperfusion injury (CIRI). Ferroptosis was confirmed by Western blotting assays, transmission electron microscopy, and glutathione assays. Propofol regulated Nrf2/Gpx4 signaling, enhanced antioxidant potential, inhibited the accumulation of lipid peroxides in CIRI-affected neurons, and significantly reversed CIRI-induced ferroptosis. Additionally, Gpx4 inhibitor RSL3 and Nrf2 inhibitor ML385 attenuated the effects of propofol on antioxidant capacity, lipid peroxidation, and ferroptosis in CIRI-affected neurons. Our data support a protective role of propofol against ferroptosis as a cause of cell death in mice with CIRI. Propofol protected against CIRI-induced ferroptosis partly by regulating the Nrf2/Gpx4 signaling pathway. These findings may contribute to the development of future therapies targeting ferroptosis induced by CIRI.
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