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pubmed, article, google, scholar, ferroptosis, iron, nrf, cell, gpx, acupuncture, central, fth, cas, expression, cerebral, rats, group, therapy, fig, data, intracerebral, protein, injury, model, pathway, liu, neurological, cells, hemorrhage, zhang, wang, nerve, keap, death, nuclear, demonstrated, oxidative, days, damage, sham, antioxidant, lipid, brain, day, chen, sun, cohort, research, scalp, china,

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tryparedoxin peroxidase-deficiency commits trypanosomes nrf2-keap1 pathway promotes cell proliferation disease drug candidates identifies sterubin post-stroke shoulder-hand syndrome article download pdf neuronal ferroptosis protects hemorrhagic brain p62-keap1-nrf2 pathway protects mincle/syk signalling cascade transfusion-dependent thalassemia syndromes p62-keap1-nrf2 antioxidant pathway baihui acupoint-penetrating-qubin acupoint gel-pro-analyzer software reactive oxygen species multi-purpose scaffold protein p62/keap1/nrf2 pathway implicated keap1-dependent degradative ubiquitination blood-brain barrier disruption central nervous system patient-derived keap1 mutations peri-haemorrhagic tissues compared ich-induced neurological deficits p62-dependent phase separation porus acusticus externus iron-rich cells compared rehabilitation training combined acupuncture tyurina nano-targeted induction peri-haemorrhagic cerebral tissues nlrp3 inflammasome pathway p62-keap1-nrf2 pathway p62/keap1/nrf2 pathway de gregorio-rocasolano longitudinal mitochondrial axis ferroptosis-type cell death national research council nrf2-governed antioxidant pathways funding body played mitigating lipid peroxidation dependent transcription factor enhancing nuclear accumulation privacy choices/manage cookies semi-quantitative data relating nerve cell bodies surplus iron accumulation xin-yang yu full access mitochondrial structural change mitochondrial morphological characteristics nrf2-dependent pathway autophagy increases susceptibility nerve cell body

Questions {❓}

• Kang R, Tang D (2017) Autophagy and ferroptosis - what’s the connection?
• Toyokuni S (2014) Iron and thiols as two major players in carcinogenesis: friends or foes?

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         headline:Scalp Acupuncture Protects Against Neuronal Ferroptosis by Activating The p62-Keap1-Nrf2 Pathway in Rat Models of Intracranial Haemorrhage
         description:Intracerebral haemorrhage (ICH) can be a catastrophic event; even if the initial stages of the pathology were well-managed, a number of patients experience varied residual neurological deficits following the insult. Ferroptosis is a recently identified type of cell demise which is tightly linked to the neurological impairment associated with ICH. In the current work, the prophylactic impact of scalp acupuncture (SA) therapy on autologous blood injection murine models of ICH was investigated in order to establish whether SA could mitigate the secondary damage arising following ICH by moderating ferroptosis. The pathophysiological mechanisms associated with this process were also explored. Ludmila Belayev tests were utilised for the characterisation of neurological damage. Haematoxylin–eosin staining was employed in order to determine the cerebral impact of the induced ICH. Malondialdehyde (MDA) and iron titres in peri-haemorrhagic cerebral tissues were appraised using purchased assay kits. Transmission electron microscopy delineated mitochondrial appearances within nerve cell bodies from the area of haemorrhage. Western blotting techniques were utilised to assay the degree of protein expression of NeuN, sequestosome 1 (p62), nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (Keap1), glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1). The frequencies of Nrf2, GPX4 and FTH1 positive cells, respectively, were documented with immunohistochemical staining. The results demonstrated that therapy with SA after ICH mitigated MDA and iron sequestration, diminished the appearance of contracted mitochondria with increased outer mitochondrial membrane diameter within the nerve cell bodies, and suppressed neuronal ferroptosis. The pathways responsible for these effects may encompass amplified p62, Nrf2, GPX4 and FTH1 expression, together with decreased Keap1 expression. Application of SA reduced identified neurobehavioural abnormalities after ICH; no disparities were observed between the consequences of SA therapy and deferoxamine delivery. It can be surmised that intervention with SA enhanced recovery after ICH by triggering the antioxidant pathway, p62/Keap1/Nrf2, and causing FTH1 and GPX4 upregulation, factors that participate in diminishing excess iron and thus in mitigating lipid peroxidation insults arising from ferroptosis following ICH.
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      headline:Scalp Acupuncture Protects Against Neuronal Ferroptosis by Activating The p62-Keap1-Nrf2 Pathway in Rat Models of Intracranial Haemorrhage
      description:Intracerebral haemorrhage (ICH) can be a catastrophic event; even if the initial stages of the pathology were well-managed, a number of patients experience varied residual neurological deficits following the insult. Ferroptosis is a recently identified type of cell demise which is tightly linked to the neurological impairment associated with ICH. In the current work, the prophylactic impact of scalp acupuncture (SA) therapy on autologous blood injection murine models of ICH was investigated in order to establish whether SA could mitigate the secondary damage arising following ICH by moderating ferroptosis. The pathophysiological mechanisms associated with this process were also explored. Ludmila Belayev tests were utilised for the characterisation of neurological damage. Haematoxylin–eosin staining was employed in order to determine the cerebral impact of the induced ICH. Malondialdehyde (MDA) and iron titres in peri-haemorrhagic cerebral tissues were appraised using purchased assay kits. Transmission electron microscopy delineated mitochondrial appearances within nerve cell bodies from the area of haemorrhage. Western blotting techniques were utilised to assay the degree of protein expression of NeuN, sequestosome 1 (p62), nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (Keap1), glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1). The frequencies of Nrf2, GPX4 and FTH1 positive cells, respectively, were documented with immunohistochemical staining. The results demonstrated that therapy with SA after ICH mitigated MDA and iron sequestration, diminished the appearance of contracted mitochondria with increased outer mitochondrial membrane diameter within the nerve cell bodies, and suppressed neuronal ferroptosis. The pathways responsible for these effects may encompass amplified p62, Nrf2, GPX4 and FTH1 expression, together with decreased Keap1 expression. Application of SA reduced identified neurobehavioural abnormalities after ICH; no disparities were observed between the consequences of SA therapy and deferoxamine delivery. It can be surmised that intervention with SA enhanced recovery after ICH by triggering the antioxidant pathway, p62/Keap1/Nrf2, and causing FTH1 and GPX4 upregulation, factors that participate in diminishing excess iron and thus in mitigating lipid peroxidation insults arising from ferroptosis following ICH.
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         Scalp acupuncture
         Ferroptosis
         p62
         Nrf2
         GPX4
         FTH1
         Neurosciences
         Neurochemistry
         Cell Biology
         Proteomics
         Neurology
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      name:Heilongjiang University of Chinese Medicine, Harbin, China

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