Evidence map›Paper›PMID 42246542›Full record

ArticleInvestigative ophthalmology & visual science2026

Diosgenin Attenuates Photoreceptor Degeneration in an N-Methyl-N-Nitrosourea-Induced Mouse Model of Retinal Degeneration.

Wanqing Tong, Jinfeng Cao, Xuebin Zhou, Bo Jia, Dan Li, Jinling Fu

Abstract read
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Article in Investigative ophthalmology & visual science, 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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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Wanqing TongDepartment of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.
Jinfeng CaoDepartment of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.
Xuebin ZhouDepartment of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.
Bo JiaDepartment of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.
Dan LiDepartment of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.
Jinling FuDepartment of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Retinitis pigmentosa (RP) is a hereditary retinal disorder distinguished by progressive photoreceptor cell (PRC) loss, in which glial activation can accelerate degeneration. Diosgenin, a natural steroidal sapogenin with potent anti-inflammatory properties, has shown therapeutic potential for ocular and neurodegenerative diseases but has not been explored for retinal degeneration. This study examined the protective role of diosgenin against PRC degeneration and explored potential anti-inflammatory mechanisms in an N-methyl-N-nitrosourea (MNU)-induced mouse model of retinal degeneration. Methods: The model was established by intraperitoneal injection of 50 mg/kg MNU, followed by oral gavage of diosgenin/lutein (positive control)/vehicle. The effects of diosgenin on PRC structure, apoptosis, retinal function, and glial activation were evaluated. Network pharmacology and molecular docking were used to investigate potential mechanisms. Results: Diosgenin preserved retinal integrity and function in MNU-induced mice, with relative preservation of the outer nuclear layer thickness and outer segment (OS) length of rods and cones. Disorganization of OS membrane discs and abnormal morphology of organelles were attenuated, while fundus photographs showed fewer lesions. Furthermore, diosgenin mitigated PRC apoptosis and maintained retinal light responses. Mechanistically, diosgenin ameliorated reactive gliosis of Müller glial cells (MGCs), attenuated the expression levels of inflammatory cytokines and chemokines, and mitigated activation of the IL6ST/JAK2/STAT3 pathway. Conclusions: Diosgenin attenuated PRC degeneration in MNU-induced mice, and one of its mechanisms may involve the attenuation of reactive gliosis in MGCs and inflammatory responses, with possible involvement of the IL6ST/JAK2/STAT3 pathway. Diosgenin may serve as a potential intervention candidate for retinal degenerative diseases, such as RP.

Indexed as

DiosgeninPhotoreceptor Cells, VertebrateRetinal DegenerationAnimalsApoptosisBlotting, WesternDisease Models, AnimalJanus Kinase 2MaleMethylnitrosoureaMiceMice, Inbred C57BLSTAT3 Transcription FactorDiosgeninJak2 protein, mouseJanus Kinase 2MethylnitrosoureaStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID42246542
PMCPMC13249205

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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.