ArticleNutrients2025
Exploring the Neuroprotective Properties of Capsanthin: Antioxidant Defense and Inflammatory Responses.
Article in Nutrients, 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
8 authors.
Funding
Abstract
BACKGROUND/
objectivesCapsanthin is a xanthophyll carotenoid from Capsicum species with an extended conjugated polyene chain that underlies both its orange-red color and strong antioxidant potential. In this study, we investigated whether capsanthin protects RA-differentiated SH-SY5Y neuron-like cells against glutamate-induced stress.
methodsNeuronal dysfunction was induced by glutamate exposure, and capsanthin treatment was evaluated using cell viability, reactive oxygen species (ROS) production, antioxidant defense markers, inflammatory cytokines, mitochondrial energy status, and apoptosis-related endpoints. Antioxidant responses were assessed using superoxide dismutase, catalase, glutathione peroxidase activities, and total antioxidant capacity. Cytokine release (TNFα, IL-6, IL-8, IL-4, IL-10) was quantified by ELISA. Mitochondrial function was monitored using ATP content. Apoptosis-associated genes (BAX, BCL-2, CASP3, and CASP9) were analyzed using SYBR Green-based RT-qPCR, complemented by caspase-9 ELISA and caspase-3 Western blotting.
resultsGlutamate increased oxidative stress and shifted the cytokine profile toward a pro-inflammatory state, accompanied by reduced ATP levels and a pro-apoptotic transcriptional pattern. Capsanthin significantly attenuated glutamate-induced ROS production, stabilized antioxidant enzyme activities and total antioxidant capacity, reduced pro-inflammatory cytokines while supporting anti-inflammatory signaling, and preserved ATP levels.
conclusionsOverall, capsanthin mitigated excitotoxic stress by maintaining redox balance, limiting inflammatory responses, and protecting mitochondrial energy metabolism in neuron-like cells, supporting its potential as a neuroprotective candidate for glutamate-induced neuronal stress.
Indexed as
Identifiers
What 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.