ArticleJournal of bioenergetics and biomembranes2025
Mollugin attenuates oxygen-glucose deprivation/reperfusion-induced brain microvascular endothelial cell death and permeability through activation of BDNF/TrkB-modulated Akt pathway.
Article in Journal of bioenergetics and biomembranes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Mollugin: A Comprehensive Review of Its Multifaceted Pharmacological Properties and Therapeutic Potential.International journal of molecular sciences · 2025Review
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
Brain microvascular endothelial cell injury is an important pathological basis for blood-brain barrier damage in ischemic stroke. Mollugin is a bioactive phytochemical constituent from Rubia cordifolia L., which has a protective potential in some diseases. However, the biological mechanism of mollugin in cerebrovascular damage in ischemic stroke is unknown. Human brain microvascular endothelial cells (hBMECs) were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to mimic the cerebrovascular damage in ischemic stroke. Cell viability was measured via MTT. Cell death was evaluated via flow cytometry, LDH release assay, and western blotting. Cell permeability was examined via FITC-dextran permeability assay and western blotting. Mollugin mitigated OGD/R-induced viability reduction of hBMECs. Moreover, mollugin attenuated OGD/R-induced increase in apoptotic rate, LDH release, and cleaved caspase-3 level and decrease in Bcl-2 level. Furthermore, mollugin attenuated OGD/R-induced increase in permeability and decrease in Zonula occludens-1 (ZO-1) and Claudin-5 levels. In addition, mollugin mitigated OGD/R-induced BDNF/TrkB and Akt pathways. BDNF or Akt knockdown reversed the protective effects of mollugin on cell death and permeability of hBMECs. The findings suggest that mollugin attenuates cell death and permeability of hBMECs induced by OGD/R through activating BDNF/TrkB-modulated Akt pathway.
Indexed as
Identifiers
40445497What 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.