ArticleFrontiers in pharmacology2025
Article in Frontiers in pharmacology, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Solar ultraviolet A (UVA) induces skin photodamage primarily by triggering endoplasmic reticulum (ER) stress, leading to misfolded protein accumulation and apoptosis. Methods: We characterized CT metabolites using UPLC-ESI-MS/MS, identifying 1,288 metabolites with flavonoids as predominant. The anti-UVA effects of CT in human keratinocytes (HaCaT) were assessed via bulk mRNA sequencing, Western blot analysis, immunofluorescence, flow cytometry, and siRNA-mediated knockdown of Nrf2. Results: CT contains numerous flavonoids that contribute to its antioxidative capacity. In UVA-exposed HaCaT cells, CT significantly reduced apoptosis, inflammatory cytokine release, and reactive oxygen species (ROS) production. It downregulated ER stress markers (CHOP, pIRE1, ATF6), preserved ER morphology, and decreased downstream apoptotic signaling. Nrf2 knockdown experiments revealed that CT's protective effects depend on Nrf2-mediated antioxidant responses. Conclusion: CT alleviates UVA-induced skin photodamage by concurrently inhibiting all three branches of ER stress and activating Nrf2-driven antioxidant defenses, thereby modulating apoptosis. These findings position CT as a promising natural agent for dermocosmetic and therapeutic strategies against UVA-mediated skin injury.
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.