ArticleJournal of natural medicines2026
Protopanaxatriol ameliorates diabetic retinopathy by regulating mTOR/G6PD mediated pentose phosphate pathway.
Article in Journal of natural medicines, 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
In traditional Chinese medicine (TCM), Panax notoginseng and Panax notoginseng saponins (PNS) have been widely used to treat diabetic retinopathy (DR), but the material basis remains to be elucidated. This study aims to investigate the pharmacological effects and underlying mechanisms of protopanaxatriol (PPT), a main metabolite of PNS, in the treatment of DR. UPLC-MS/MS was employed to identify the metabolites of PNS in rats, and the metabolite PPT was detected in plasma, liver and intestinal contents of rats after oral administration of PNS. Different concentrations of PPT could significantly inhibit the proliferation, cell migration and tube formation of hRMECs induced by high-glucose in vitro and reduce the retinal vessel diameters of Tg (Fli1a: EGFP) zebrafish larvae, which were dilated by 130 mmol/L glucose in vivo. Cellular metabolomics revealed that PPT modulated the pentose phosphate pathway of hRMECs in high glucose. Further research indicates that PPT significantly reduced the G6PD activity and decreased the phosphorylation of mTOR in high glucose-induced hRMECs. In conclusion, PPT, a main metabolite of PNS, could effectively ameliorate DR by regulating the mTOR/G6PD-mediated pentose phosphate pathway, which may provide scientific data for elucidating the material basis of PNS in treating DR.
Indexed as
Identifiers
41735621What 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.