ArticleJournal of cellular and molecular medicine2025
Plantamajoside Promotes NGF/TrkA Pathway to Inhibit Neuronal Apoptosis and Improve Diabetic Peripheral Neuropathy.
Article in Journal of cellular and molecular medicine, 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.
- Black phosphorus nanosheet-enabled ROS-adaptive core-shell microneedles orchestrate immunoredox remodeling and neurotrophic regeneration for facial nerve repair.Journal of nanobiotechnology · 2026Article
- PPM1A dysfunction aggravates DPN pathology through NF-κB/NLRP3/p-tau axis involving Schwann cell/DRG neuron crosstalk.Journal of translational medicine · 2026Article
- Research progress on targeting autophagy pathways with medicinal plants and their active metabolites for the treatment of heart failure.Frontiers in pharmacology · 2026Review
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
The symptoms caused by diabetic peripheral neuropathy (DPN) have severely impacted patients' quality of life. While plantamajoside (PMS) exhibits neuroprotective properties, its efficacy and molecular mechanisms against DPN are unexplored. This study first established a high glucose (HG)-induced in vitro model of DPN and investigated the neuroprotective effects of PMS on RSC96 cells. We next demonstrated the anti-apoptotic effects of PMS and NGF/TrkA pathway mediated neurotrophic effects. Finally, we established a DPN mouse model and confirmed the therapeutic effects of PMS on DPN mice through behavioural tests and pathological staining, while also assessing the impact of PMS on the NGF/TrkA pathway and apoptosis. Our results showed that, in HG-induced DPN models, PMS enhanced cell viability while reducing LDH activity. Transcriptomics results indicated that the Apoptosis and Neurotrophins signalling pathways were key pathways for PMS on DPN. PMS treatment reduced HG-induced RSC96 cell apoptosis while enhancing NGF levels and upregulating NGF/TrkA-related protein expression. However, this protection was abolished by TrkA inhibitor or NGF neutralising antibodies. In vivo experimental results showed that PMS improved the mechanical pain threshold, thermal pain reaction time, and nerve conduction velocity of DPN mice. PMS improved pathological damage to the sciatic nerve, enhanced the number of Nissl bodies, reduced TUNEL-positive expression, and upregulated NGF levels. Furthermore, PMS reduced apoptosis and elevated NGF/TrkA-related protein expression in the sciatic nerve of DPN mice. In conclusion, PMS alleviates DPN through activating the NGF/TrkA pathway and inhibiting apoptosis.
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.