ArticleInflammation2025
Effects of Troxerutin on Oxidative Stress, Inflammation and Galectin- 3 Expression in Intracerebroventricular Kainic Acid-Induced Neurotoxicity.
Article in Inflammation, 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
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
4 citing papers in PubMed.
- Troxerutin suppresses the stemness of hepatocellular carcinoma via the Syk/FOXO3 feedback loop.Cell biology and toxicology · 2026Article
- Exosomes in inflammatory tissue injury: key pathogenic factors and promising therapeutic agents.Frontiers in immunology · 2026Review
- Tie2-mediated CBL ubiquitination of EGFR underlies ultrasound-responsive silk fibroin/graphene oxide hydrogel-troxerutin therapy for intervertebral disc degeneration.Materials today. Bio · 2025Article
- Immunohistochemical examination of CD163 and TROP2 expression levels in ovarian endometriosis.Journal of molecular histology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Excitotoxicity caused by excessive concentration of the excitatory neurotransmitter glutamate causes neuronal cell death and promotes neurodegenerative disorders. The neuroexcitant neurotoxin kainic acid (KA) induces excitotoxicity, leading to neuronal death via oxidative stress and inflammation, and its experimental use is widespread. This study was designed to determine the protective effect of Troxerutin (TXR) and its relationship with Galectin-3 (Gal-3) in experimental excitotoxicity with neuroinflammation and oxidative stress. Fifty male Wistar rats were divided into five groups (n = 10): Control group rats received intraperitoneal (ip) normal saline for 6 days. Sham group rats received a single dose of intracerebroventricular (icv) normal saline on the first day. KA group rats were treated with a single dose of KA; icv-0.5 μg/μl). TXR group rats treated with TXR for 6 days: ip-100 mg/kg) and KA + TXR group rats treated with KA (single dose) and TXR (6 days). It was observed that malondialdehyde (MDA) and interleukin-1β (IL-1β) levels increased and reduced glutathione (GSH) levels decreased in the cerebral cortex of rats with KA neurotoxicity. TXR treatment caused a significant improvement in MDA and GSH levels and a significant decrease in IL-1β levels in rats with the excitotoxicity model. Gal-3 expressions in the hippocampus and cerebellum increased in KA-treated rats, whereas TXR treatment decreased Gal-3 expressions. In addition, histopathological changes caused by KA administration showed improvement in TXR-treated groups. In conclusion, the findings showed that TXR treatment attenuated KA-induced neurotoxicity by reducing oxidative tissue damage, inflammatory response and Gal-3 expression.
Indexed as
Identifiers
What 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.