Article3 Biotech2025
Indole 3 carbinol attenuated memory impairment, oxidative stress, inflammation, and apoptosis in bilateral common carotid artery occlusion induced brain damage in rats.
Article in 3 Biotech, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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
1 citing paper in PubMed.
- Unveiling the Multifaceted Pharmacological Actions of Indole-3-Carbinol and Diindolylmethane: A Comprehensive Review.Plants (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Global cerebral ischemia (GCI) is associated with a multifaceted etiology, including increased oxidative stress, inflammation, and elevated acetylcholinesterase (AChE) activity, ultimately leading to cognitive and memory impairments. This study aimed to evaluate the neuroprotective, cognitive, and memory-enhancing effects of indole 3-carbinol (I3C), a phytochemical found in cruciferous vegetables. Additionally, network pharmacology analyses were conducted to identify potential molecular targets of I3C in GCI. Bilateral common carotid artery occlusion (BCCAO) surgery was performed to induce GCI. I3C was administered orally for 14 days, and cognitive and memory functions were assessed using the Y-maze and Morris water maze paradigms. Biomarkers of oxidative stress (MDA, Nrf2, SOD, and CAT), inflammatory markers (NF-κB, TNF-α, and IL-10), and AChE enzyme activity were evaluated. The results demonstrated that I3C treatment significantly inhibited AChE activity, improved spontaneous alternation (%) in the Y-maze test, increased the number of entries and time spent in the platform zone, and reduced escape latency in the Morris water maze test, indicating enhanced cognitive and memory functions. I3C treatment also increased brain levels of Nrf2, SOD, and CAT while reducing MDA levels. Furthermore, it decreased pro-inflammatory markers such as NF-κB and TNF-α and elevated the anti-inflammatory marker IL-10, suggesting neuroprotection through the mitigation of oxidative stress and inflammation. Histopathological analysis revealed improved integrity of CA1 neurons in BCCAO rats treated with I3C. Network pharmacology studies identified TP53, AKT1, TNF, STAT3, BCL2, SRC, ESR1, CCND1, CASP8, and CASP3 as the top ten molecular targets for I3C in the context of GCI. Our in vivo data, supported by network pharmacology studies, suggest that I3C's neuroprotective and cognitive-enhancing effects are driven by its ability to alleviate oxidative stress, inflammation, and apoptosis. Overall, this study suggests that I3C is a promising neuroprotective and memory-enhancing agent for global cerebral ischemia.
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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 Socratic graph.