ArticleNeuromolecular medicine2025
Neuroprotective Activity of Eriodictyol Against Streptozotocin-Induced Diabetic Peripheral Neuropathy in Wistar Rats by Targeting Wnt/β-Catenin Pathway.
Article in Neuromolecular medicine, 2025. 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term hyperglycemia and insulin dysfunction deteriorate peripheral nerve functions, leading to sensory loss, spontaneous pain, and hypersensitivity (i.e., allodynia and hyperalgesia). Evidence indicates glucose-induced upregulation of the Wnt/β-catenin mechanism in diabetic peripheral neuropathy (DPN). Eriodictyol (Ed) has shown protective effects against glucotoxicity. The present study explored the bioactivity of Ed in streptozotocin (STZ) induced DPN and the role of the Wnt/β-catenin pathway. Ed or gabapentin (Gpn), or methyl vanillate (MV) was administered in Wistar rats for 4 weeks, starting 6 weeks after STZ administration. Ed ameliorated the mean body weight and mitigated polydipsia and polyphagia in DPN rats. The data indicated that Ed attenuated hyperglycemia, glycosylated hemoglobin (HbA1c) levels, and HOMA-IR, and enhanced circulating insulin levels and HOMA-β against STZ-induced DPN. MV (Wnt/β-catenin activator) caused a significant increase in STZ-induced hyperglycemia, HbA1c, HOMA-IR, and further decreased the insulin levels and HOMA-β in STZ-treated rats. Ed attenuated oxidative stress, inflammatory expression, level of advanced glycation end products, and nuclear factor kappa B in the sciatic nerve of STZ-treated neuropathic rats, and MV further potentiated these markers triggered by STZ. Interestingly, Ed and Gpn attenuated mRNA expression of Wnt1/β-catenin in the sciatic nerve of neuropathic rats. Hyperalgesia and allodynia were significantly ameliorated in Ed or Gpn-treated rats against DPN. Furthermore, Ed ameliorated the biochemical biomarkers, histopathological characteristics, and nociceptive-like responses in STZ and MV-treated rats. It is concluded that Ed can alleviate the pathogenic course of DPN. Wnt/β-catenin pathway might be involved in the eriodyctiol-triggered mitigation of nociceptive-like responses in diabetic rats.
Indexed as
Identifiers
40856886What 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.