ArticleFrontiers in pharmacology2026
Neuroprotective effects of curcumin, memantine, and caffeic acid in a Rat model of cerebral ischemia-reperfusion injury.
Article in Frontiers in pharmacology, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia-reperfusion (I/R) injury leads to neuronal loss through oxidative stress, inflammation, and apoptosis. Curcumin, memantine, and caffeic acid possess antioxidant and neuroprotective properties. This study compared their efficacy in a rat model of transient cerebral ischemia. Forty male Wistar albino rats were initially allocated into six experimental groups; however, the vehicle control group was excluded from statistical analyses, and data are presented for five groups (n = 8 per group): sham, ischemia-reperfusion (I/R), I/R + curcumin (300 mg/kg/day), I/R + memantine (10 mg/kg/day), and I/R + caffeic acid (10 μmol/kg/day). Transient ischemia was induced by bilateral carotid artery occlusion for 30 min followed by 72 h reperfusion. Treatments were administered intraperitoneally beginning 30 min after reperfusion and continued once daily for five consecutive days. Histopathological and immunohistochemical analyses of the frontoparietal cortex demonstrated that I/R induced severe neuronal degeneration, necrosis, gliosis, vascular hyperemia, and marked inflammatory and apoptotic activation, with severity scores reaching the highest grade (3) (p < 0.001 vs. sham). Memantine and caffeic acid significantly reduced all degenerative, inflammatory, and apoptotic parameters (p < 0.001), restoring histopathological morphology to levels not statistically different from the sham group (p > 0.05). In particular, caspase-3, IL-1β, TNF-α, and TUNEL positivity were markedly suppressed in both treatment groups. In contrast, curcumin treatment resulted in only partial attenuation of neuronal degeneration and inflammatory infiltration, without achieving statistical significance in most parameters (p > 0.05 vs. I/R). Correlation analyses revealed strong negative associations between antioxidant enzyme activities (GR and GST) and histopathological damage scores (r = -0.71 to -0.82, p < 0.001), as well as strong positive correlations between apoptotic/inflammatory markers and neuronal injury severity (r = 0.68 to 0.79, p < 0.001). These findings demonstrate that memantine and caffeic acid exert robust histopathological neuroprotection against cerebral ischemia-reperfusion injury, whereas curcumin shows limited efficacy under the applied experimental conditions.
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.