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Published on: January 21, 2018
Intravitreal nintedanib attenuates proliferative vitreoretinopathy in a mouse model: Efficacy, safety, and
Elif Bağatur Vurgun1, Mehmet Orkun Sevik2, Aslan Aykut2
1Department of Ophthalmology, Kandıra Kazım Dinç State Hospital, Kocaeli, Türkiye.
Background:
To evaluate the efficacy and safety of intravitreal injection of the multityrosine kinase inhibitor nintedanib (NTB) in a mouse model of proliferative vitreoretinopathy (PVR) induced by dispase.
Methods:
Fifty-two male C57BL/6 mice received intravitreal injections in the right eye and were divided into four groups: PVR, PVR + NTB, NTB-only, and vehicle. Uninjected contralateral eyes served as a healthy-control group. The PVR and PVR + NTB groups were compared based on clinical and histopathological PVR grading. Immunohistochemistry, ELISA, RT-PCR, and Western blot analyses were used to evaluate and compare markers of inflammation, fibrogenesis, and epithelial-mesenchymal transition between PVR, PVR + NTB, and healthy-control groups. Potential retinal toxicity was assessed using electroretinography and histopathology in the NTB-only and vehicle groups.
Results:
Clinical PVR grades were significantly lower in the PVR + NTB group (0.65 ± 0.93) than in the PVR group (2.70 ± 1.75) (p < 0.001). Histopathological grading was also significantly lower in the PVR + NTB group (1.62 ± 0.91) compared with the PVR group (3.87 ± 1.24) (p = 0.002). Compared with the PVR group, IL-6, PDGF, TGF-β, and TNF-α levels, as well as acta-2, col1a1, and fn-1 mRNA expression were significantly lower in the PVR + NTB group. Phosphorylated-PDGFR-α levels were also reduced, whereas PDGFR-α protein expression remained unchanged. No signs of retinal toxicity were observed in electroretinography or histopathology.
Conclusions:
In this mouse PVR model, intravitreal NTB reduced clinical, histopathological, and biochemical manifestations of PVR without detectable toxicity. Intravitreal NTB may represent a promising therapeutic option for the management of PVR.
Insights
Intravitreal nintedanib (NTB) effectively reduced proliferative vitreoretinopathy (PVR) in a mouse model. This study found NTB to be a safe and promising treatment for PVR, showing no detectable retinal toxicity.
Area of Science:
- Ophthalmology
- Retinal Diseases
- Pharmacology
Background:
- Proliferative vitreoretinopathy (PVR) is a severe complication of retinal detachment.
- Current treatments for PVR have limitations, necessitating novel therapeutic approaches.
- Nintedanib (NTB), a multityrosine kinase inhibitor, has potential anti-fibrotic and anti-inflammatory properties.
Purpose of the Study:
- To evaluate the efficacy and safety of intravitreal nintedanib (NTB) in a dispase-induced mouse model of proliferative vitreoretinopathy (PVR).
- To assess the impact of NTB on PVR development, inflammation, fibrogenesis, and epithelial-mesenchymal transition.
- To determine potential retinal toxicity associated with intravitreal NTB administration.
Main Methods:
- Fifty-two male C57BL/6 mice were used, with intravitreal injections in the right eye.
- Groups included: PVR, PVR+NTB, NTB-only, and vehicle; uninjected eyes served as controls.
- Evaluations involved clinical and histopathological PVR grading, immunohistochemistry, ELISA, RT-PCR, Western blot, electroretinography, and histopathology.
Main Results:
- Intravitreal NTB significantly reduced both clinical and histopathological PVR grades compared to the PVR group (p<0.001 and p=0.002, respectively).
- NTB treatment lowered levels of inflammatory markers (IL-6, TNF-α) and fibrogenic factors (PDGF, TGF-β), and reduced mRNA expression of acta-2, col1a1, and fn-1.
- No retinal toxicity was observed via electroretinography or histopathology in NTB-treated eyes.
Conclusions:
- Intravitreal nintedanib (NTB) demonstrated significant efficacy in reducing clinical, histopathological, and biochemical markers of PVR in a mouse model.
- NTB was well-tolerated, with no detectable retinal toxicity observed.
- Intravitreal NTB shows promise as a novel therapeutic strategy for managing proliferative vitreoretinopathy.
