Evidence map›Paper›PMID 41929257›Full record

ArticleFrontiers in pharmacology2026

Anxiolytic and antidepressant effects of astaxanthin: behavioral and mechanistic insights in a rat model.

Mohammad Ranjbari, Sajad Fakhri, Fatemeh Abbaszadeh, Amir Kiani, Ehsan Mohammadi-Noori, Javier Echeverría

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Mohammad RanjbariStudent Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Sajad FakhriPharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Fatemeh AbbaszadehNeurobiology Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Amir KianiPharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Ehsan Mohammadi-NooriPharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Javier EcheverríaDepartamento de Ciencias del Ambiente, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, Chile.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Astaxanthin (AST) is a potent carotenoid with antioxidant properties that has garnered attention for its potential neuropharmacological effects. Purpose: This study investigates the anxiolytic and antidepressant activities of AST in a rat model to elucidate its therapeutic potential for mood disorders. Material and Methods: Fifty-four male rats were divided into nine groups receiving normal saline, astaxanthin (AST, 5, 10, and 15 mg/kg), diazepam (DZP, 0.5 mg/kg), fluoxetine (FXT, 5 mg/kg), or combinations of AST (10 mg/kg) with receptor antagonists flumazenil (FLU, GABA-A antagonist), atropine (ATR, muscarinic antagonist), and naloxone (NAL, opioid antagonist) for 14 consecutive days. At the end of the study, behavioral assessments were conducted, including the open field, light-dark box, elevated plus maze, tail suspension, and forced swimming tests. Biochemical analyses were performed to evaluate serum catalase (CAT), glutathione (GSH), nitrite, and matrix metalloproteinase-2 (MMP-2) and MMP-9 activities. Results and Discussion: Astaxanthin, particularly at 10 mg/kg, significantly reduced anxiety- and depressive-like behaviors, comparable to DZP and FXT in four-week-old male Wistar rats. Pretreatment with FLU, ATR, or NAL partially reversed these effects, suggesting involvement of GABAergic, cholinergic, and opioid pathways. Furthermore, AST enhanced antioxidant defenses, evidenced by increased serum CAT and GSH levels and reduced nitrite concentrations. Gelatin zymography revealed that AST increased MMP-2 activity while slightly decreasing MMP-9 activity, a partial reversal by the aforementioned antagonists. Conclusion: The results suggest that AST could produce anxiolytic and antidepressant effects. Such effects are likely mediated through GABAergic, cholinergic, and opioid systems, as well as antioxidant and anti-inflammatory mechanisms. Future studies should focus on well-controlled clinical trials to evaluate the preclinical results.

Indexed as

anxietyastaxanthindepressionGABAergic systemmuscarinic acetylcholine receptorsopioid system

Identifiers

PMID41929257
PMCPMC13038905

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Registered trials

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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.