ArticleLife (Basel, Switzerland)2026
Effects of Dexmedetomidine Treatment After Cerebral Ischemia/Reperfusion on Apoptosis and Oxidative Stress: A Rat Model.
Article in Life (Basel, Switzerland), 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesCerebral ischemia/reperfusion (IR) injury is characterized by excessive oxidative stress and activation of apoptotic pathways, which play a central role in neuronal loss and poor neurological outcomes. Modulation of these mechanisms represents a clinically relevant strategy for neuroprotection. This study aimed to investigate the neuroprotective effects of dexmedetomidine (Dex) on oxidative stress, apoptotic signaling, and neuronal integrity in an experimental rat model of cerebral IR injury. MATERIALS AND
methodsFemale Wistar rats were assigned to control, IR, and IR+Dex groups. Transient cerebral ischemia was induced for 45 min followed by 2 h of reperfusion. Oxidative stress was evaluated using serum antioxidant enzyme activities (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH-Px]), total oxidant and antioxidant status (TOS, TAS), and lipid peroxidation levels (malondialdehyde [MDA]). Apoptotic signaling was assessed by histopathological examination, transmission electron microscopy, and immunohistochemical analysis of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and apoptotic peptidase activating factor-1 (APAF-1) expression, quantitatively evaluated using QuPath with statistical comparison between groups. Bioinformatic network analysis and molecular docking were performed to explore predicted interactions between Dex and apoptosis-related proteins.
resultsCerebral IR induced a marked oxidative imbalance, characterized by reduced antioxidant enzyme activities and increased lipid peroxidation. Dex treatment partially improved antioxidant capacity and reduced oxidative stress parameters. Histopathological and ultrastructural analyses demonstrated severe neuronal degeneration following IR, whereas Dex-treated rats exhibited attenuated neuronal damage and improved ultrastructural preservation. Immunohistochemical analysis showed increased Bax and APAF-1 expression and reduced Bcl-2 expression after IR; these alterations were significantly modulated toward control levels in the IR+Dex group. Bioinformatic analysis identified apoptosis-related pathways, including apoptosis, p53 signaling, and necroptosis, as significantly enriched, while molecular docking suggested stable predicted interactions between Dex and key apoptotic regulators.
conclusionsIn this experimental rat cerebral IR model, Dex exerted partial but significant neuroprotective effects by attenuating oxidative stress, modulating apoptotic marker expression, and preserving neuronal morphology. These findings support the potential role of Dex as a neuroprotective agent in ischemia-related brain injury, warranting further translational investigation.
Indexed as
Identifiers
What Socratic 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 Socratic graph.