ArticleScientific reports2026
Nrf2 attenuates neuroinflammatory injury in intracerebral hemorrhage via an ASK1/JNK-related signaling pathway.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Intracerebral hemorrhage (ICH) is a clinically prevalent cerebrovascular disorder in which neuroinflammation is a major contributor to secondary brain injury. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator of intracellular redox homeostasis, whereas apoptosis signal-regulating kinase 1 (ASK1) is involved in stress-associated inflammatory and apoptotic signaling. However, the relationship between Nrf2 signaling and ASK1/JNK pathway activity in ICH-related inflammatory injury remains incompletely understood. In this study, we established a rat ICH model and used molecular, histological, and behavioral approaches to examine the association between Nrf2 signaling and ASK1/JNK-related neuroinflammatory changes. We found that ICH was accompanied by increased Nrf2 and phosphorylated ASK1 expression. siRNA-mediated modulation of Nrf2 or ASK1 was associated with reciprocal changes in ASK1/JNK pathway activation. In parallel, changes in CD80/CD206 expression and inflammatory cytokine levels suggested that Nrf2 signaling was associated with altered inflammation-related responses, potentially involving ASK1/JNK pathway activity. Histological analyses, including TUNEL staining, Nissl staining, and brain water content measurement, further showed that preservation of Nrf2 signaling was associated with reduced neuronal injury and cerebral edema after ICH. Behavioral assessments showed corresponding changes in locomotor and anxiety-related performance. Overall, these findings support an association between Nrf2 signaling and ASK1/JNK-related neuroinflammatory responses following ICH and provide a basis for further mechanistic investigation of this pathway in hemorrhagic brain injury.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.