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Updated: Jul 29, 2025
Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
Published on: January 12, 2022
Apigenin Alleviates Autoimmune Uveitis by Inhibiting Microglia M1 Pro-Inflammatory Polarization
Nan Shu1,2,3, Zhi Zhang4,2,3, Xiaotang Wang4,2,3
1The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Purpose:
Apigenin is a natural small molecule compound widely present in various vegetables and fruits. Recently, Apigenin was reported to inhibit lipopolysaccharide (LPS)-simulated microglial proinflammatory activation. Considering the important role of microglia in retinal disorders, we wonder whether Apigenin could exert a therapeutic effect on experimental autoimmune uveitis (EAU) through reprogramming retinal microglia to a beneficial subtype.
Methods:
EAU was induced in C57BL/6J mice by immunization with interphotoreceptor retinoid-binding protein (IRBP)651-670, followed by intraperitoneal administration of Apigenin. Disease severity was assessed based on clinical and pathological scores. In vivo, Western blotting was used to quantify protein levels of classical inflammatory factors, microglial M1/M2 markers and the tight junction protein of the blood-retinal-barrier (BRB). Immunofluorescence was used to determine the Apigenin's efficacy on microglial phenotype. In vitro, Apigenin was added in LPS and IFN-γ stimulated human microglial cell line. Western blotting and Transwell assays were used to analyze the phenotype of microglia.
Results:
In vivo, we found that Apigenin significantly reduced the clinical and pathological scores of EAU. The protein levels of inflammatory cytokines were significantly decreased in retina, and BRB disruption was ameliorated after Apigenin treatment. Meanwhile, Apigenin inhibited microglia M1 transition in EAU mice retina. In vitro functional studies showed that Apigenin decreased LPS and IFN-γ-induced microglial inflammatory factor production and M1-activation via the TLR4/MyD88 pathway.
Conclusions:
Apigenin can ameliorate retinal inflammation in IRBP induced autoimmune uveitis through inhibiting microglia M1 pro-inflammatory polarization via TLR4/MyD88 pathway.
Insights
Apigenin reduces retinal inflammation in autoimmune uveitis by reprogramming microglia. This natural compound inhibits pro-inflammatory microglial activation via the TLR4/MyD88 pathway, offering a potential therapeutic strategy.
Area of Science:
- Ophthalmology
- Immunology
- Neuroscience
Background:
- Microglia play a critical role in retinal disorders.
- Apigenin, a natural compound, inhibits pro-inflammatory microglial activation.
- Experimental autoimmune uveitis (EAU) is an inflammatory eye condition involving microglia.
Purpose of the Study:
- To investigate the therapeutic potential of Apigenin in EAU.
- To determine if Apigenin can reprogram retinal microglia to a beneficial subtype.
- To elucidate the mechanism by which Apigenin affects microglial activation in EAU.
Main Methods:
- EAU was induced in mice, followed by Apigenin administration.
- Clinical and pathological scores were used to assess disease severity.
- Western blotting, immunofluorescence, and Transwell assays were employed to analyze microglial phenotype and inflammatory markers in vivo and in vitro.
Main Results:
- Apigenin significantly reduced EAU clinical and pathological scores.
- Apigenin treatment decreased retinal inflammatory cytokines and ameliorated blood-retinal barrier disruption.
- Apigenin inhibited M1 pro-inflammatory microglial polarization in EAU mice via the TLR4/MyD88 pathway.
Conclusions:
- Apigenin ameliorates EAU by inhibiting M1 pro-inflammatory microglial polarization.
- The TLR4/MyD88 pathway is involved in Apigenin's therapeutic effect on autoimmune uveitis.
- Apigenin demonstrates potential as a therapeutic agent for retinal inflammatory diseases.
