ArticleBMJ neurology open2022
Nrf2 activation in the human brain after stroke due to supratentorial intracerebral haemorrhage: a case-control study.
Article in BMJ neurology open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Plant-Derived Natural Compounds and Nrf2-Centered Redox Signaling in Intracerebral Hemorrhage: Evidence Grading, Mechanistic Boundaries, and Translational Challenges.Antioxidants (Basel, Switzerland) · 2026Review
- Ironing out mechanisms of ferroptotic death to tailor new stroke therapies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Intracerebral haemorrhage in multiple sclerosis: assessing the impact of disease-modifying medications.European journal of medical research · 2024Review
- Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024Review
- Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke.Current neurology and neuroscience reports · 2023Review
- Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2022Review
- Review
- The Role of Concomitant Nrf2 Targeting and Stem Cell Therapy in Cerebrovascular Disease.Antioxidants (Basel, Switzerland) · 2022Review
- The Translational Potential of Microglia and Monocyte-Derived Macrophages in Ischemic Stroke.Frontiers in immunology · 2022Review
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Aims: Pharmacological activation of the antioxidative transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) improves outcomes in experimental models of intracerebral haemorrhage (ICH). However, the Nrf2 pathway has not been previously studied in humans after ICH. Our study aims to address this gap. Methods: We selected cases with fatal ICH from a prospective community-based inception cohort study and age-matched and sex-matched controls who died suddenly of non-neurological disease. We used immunohistochemistry to quantify Nrf2 (% total area stained overall and % of nuclei stained) and CD68 expression in controls and perihaematomal, ipsilateral and contralateral brain tissue from cases. We measured downstream haem oxygenase-1 (HMOX1) and NAD(P)H dehydrogenase quinone 1 [NQO1] expression using RNA in situ hybridisation. Results: 26 ICH cases (median age: 82 (IQR 76-86); 13 (50%) male) and eight controls (median age: 79 (IQR 77-80); 3 (37.5%) male) were included. We found no significant differences in overall % of Nrf2 staining between ICH cases and controls. However, the mean % of nuclei staining for Nrf2 seemed higher in perihaematomal compared with contralateral regions, although this was only statistically significant >60 days after ICH (25% (95% CI 17% to 33%) vs 14% (95% CI 11% to 17%), p=0.029). The percentage of perihaematomal tissue staining for CD68 was higher >60 days after ICH (6.75%, 95% CI 2.78% to 10.73%) compared with contralateral tissue (1.45%, 95% CI 0.93% to 1.96%, p=0.027) and controls (1.08%, 95% CI 0.20% to 1.97%, p=0.0008). RNA in situ hybridisation suggested increased abundance of HMOX1 and NQO1 transcripts in perihaematomal versus distant ipsilateral brain tissue obtained <7 days from onset of ICH. Conclusions: We found evidence of Nrf2 activation in human brain tissue after ICH. Pharmacological augmentation of Nrf2 activation after ICH might be a promising therapeutic approach.
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