ArticleHistology and histopathology2026
Therapeutic potential of porphyran in mitigating ischemia-reperfusion injury in gerbil hippocampus.
Article in Histology and histopathology, 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
7 authors.
Funding
Abstract
Cerebral ischemia-reperfusion (IR) injury is a critical pathological event that leads to extensive neuronal loss, neuroinflammation, and blood-brain barrier (BBB) dysfunction. Porphyran, a sulfated polysaccharide derived from Porphyra spp., has demonstrated anti-inflammatory and neuroprotective effects in various neurological conditions. This study aimed to evaluate the post-ischemic therapeutic potential of porphyran in a gerbil model of transient forebrain ischemia. Our findings reveal that porphyran administration (50 mg/kg orally once daily for five days) following IR significantly mitigated IR-induced cognitive decline, as evidenced by the Y-maze test, but porphyran treatment did not significantly prevent neuronal death in the CA1 subregion of the hippocampus, as revealed by Cresyl Violet (CV) and Fluoro-Jade B (FJB) staining. However, porphyran treatment after IR injury effectively attenuated the IR-induced decrease in acetylcholine (ACh) levels, suggesting potential preservation of cognitive function in surviving neurons. Furthermore, porphyran significantly mitigated microglial activation and reduced the levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), indicating its anti-inflammatory properties. Additionally, porphyran administration reduced BBB disruption, as evidenced by decreased extravasation of immunoglobulin G (IgG), suggesting a role in maintaining vascular integrity. In summary, although porphyrin administration after IR does not protect pyramidal neurons directly, it may improve cognitive function by mitigating ACh depletion, suppressing microglial activation, and reducing inflammatory cytokine levels.
Indexed as
Identifiers
40521773What 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.