Abstract
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.
Highlights
As one of the major life-threatening human pathologies, intracerebral haemorrhage (ICH) is the aetiology underpinning approximately 8–15% of cerebrovascular accidents in the United States each year (Unnithan and Mehta 2021)
Behavioural testing was conducted at 6 h and 1, 3 and 7 days following induction of ICH in order to establish the impact of scalp acupuncture (SA) on neurological impairment
Western blotting was used to assay the degree of protein expression of both nuclear factor erythroid 2-related factor 2 (Nrf2) and the downstream transcripts, glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1); the results supported the immunopositivity data (Fig. 4B, D-F). These findings indicate that FTH1 and GPX4 levels are elevated by SA via the promotion of nuclear Nrf2 accretion
Summary
As one of the major life-threatening human pathologies, intracerebral haemorrhage (ICH) is the aetiology underpinning approximately 8–15% of cerebrovascular accidents in the United States each year (Unnithan and Mehta 2021). Death rates from ICH range from 25–30% in developed nations but are 5–18% greater in less affluent states Contemporary studies have focused on the detailed analysis of iron metabolism alterations and antioxidant influences following ICH, together with ways in which to defer neuronal death by moderating intracellular metabolism and stimulating antioxidant factors. These approaches may offer potential aids to rehabilitation following this haemorrhagic cerebral insult
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