ArticleNeurochemical research2025
ALDH2 Attenuates Blood-Brain Barrier Injury Induced by Cerebral Ischemia/Reperfusion via Alleviating ROS/NLRP3 Inflammasome Axis.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed.
- Nasal-to-Brain ROS-Responsive Diselenide-Bridged Graphene Nanogel for Targeted Ischemic Stroke Therapy via Microglial Modulation.ACS omega · 2026Article
- Alcohol Interaction and ALDH2: Missing Links in EMPHASIS.Cerebrovascular diseases (Basel, Switzerland) · 2026Article
- The Molecular Mechanism of LncRNA LUCAT1 Regulating HSPB8 Expression via miR-337-3p in Modulating Neurological Damage After Cerebral Infarction.Neurochemical research · 2026Article
- ALDH2 Mediated Ferroptosis Regulation in Ischemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
An important factor influencing the prognosis of ischemic stroke is impairment of the blood-brain barrier (BBB). Additionally, oxidative stress and inflammation contribute significantly to the breakdown of the BBB during ischemic stroke reperfusion. Strong evidence suggested that Aldehyde dehydrogenase 2 (ALDH2) may have protective properties and reduce oxidative stress and inflammatory reactions in neurological conditions. Therefore, in order to examine the impact of ALDH2 on BBB integrity after ischemia/reperfusion (I/R) damage, we constructed the cerebral artery occlusion/reperfusion (MCAO/R) model and the oxygen-glucose deprivation/reperfusion (OGD/R) model. According to our findings, ALDH2 activation enhanced cell viability in bEnd.3 cells treated with OGD/R and reduced infarct area and neurological impairments in MCAO/R animals. Furthermore, both in vitro and in vivo, ALDH2 suppressed inflammation-related factors IL-1β and IL-18, as well as oxidative stress and the expression of the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome. In addition, bEnd.3 cells exhibited a reduced reactive oxygen species (ROS) generation function of ALDH2. Moreover, we noticed that ALDH2 boosted the expression of the tight junctions (TJs) zonula occludens-1 (ZO-1) and Occludin to control BBB function. In summary, ALDH2 protected against cerebral I/R injury and BBB destruction, and this protection was related to the ROS/NLRP3 axis.
Indexed as
Identifiers
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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.