Effects of Astaksanthin in experimental proliferative vitreoretinopathy

Proliferative vitreoretinopathy (PVR) is one of the most common causes of failure in retinal detachment surgery. It is characterized by membrane and contractions in the vitreous cavity, on the anterior and posterior surfaces of the retina. Today, despite the developments in vitreoretinal surgery, the desired surgical success has still not been achieved. Although PVR does not yet have a proven standard treatment modality, pharmacological treatments are still being investigated. It has been observed that these agents can increase surgical success by changing the proliferative process. Our study aims to examine the effect of astaxanthin, a member of the carotenoid family, on the developing PVR and the established PVR. In our study, 7 groups were created, each containing fourteen Sprague Dawley rats. In all groups except the control group, 0.1 ml of vitreous was aspirated by inserting a 33G needle 1.5 mm behind the limbus. No intervention was made to the rats in Group 1 (Control Group). Rats in Group 2 (Sham Group-1) were administered 0.07IU intravitreal dispase in 0.1ml and 0.1ml intravitreal DMSO solution at the beginning, 4th week and 8th week to create PVR. Rats in Group 3 (Sham Group-2) were administered 0.07IU intravitreal dispase in 0.1ml and 0.1ml intravitreal DMSO solution in the 8th week. Rats in Group 4 (Astaxanthin Group-1) were administered 0.07IU intravitreal dispase in 0.1ml and 10-ng/μL intravitreal astaxanthin at the beginning of the experiment, at the 4th week and at the 8th week. Rats in Group 5 (Astaxanthin Group-2) were administered 0.07IU intravitreal dispase in 0.1ml and 100-ng/μL intravitreal astaxanthin at the beginning of the experiment, at the 4th week and at the 8th week. Rats in Group 6 (Astaxanthin Group-3) were administered 0.07IU intravitreal dispase in 0.1ml and 10-ng/μL intravitreal astaxanthin in the 8th week. Rats in Group 7 (Astaxanthin Group-4) were administered 0.07IU intravitreal dispase in 0.1ml and 100-ng/μL dose intravitreal astaxanthin in the 8th week. A period of 8 weeks was waited for PVR development and the eyes were enucleated at the end of the period. Histopathological examination of the first 7 of 14 eyes in each group was performed. PVR stages were determined in gross pathological examination. It was evaluated histopathologically in terms of epiretinal membrane formation, presence of retinal fold and retinal detachment, subretinal fluid, cataract and uveitis. TGF-ß, PDGF, FGF, VEGF, IL-1 levels were evaluated in the other 7 of 14 eyes in each group by ELISA method. As a result, we showed that in the emerging PVR model, astaxanthin did not show any improvement in biochemical markers at both doses, but 100-ng/μL astaxanthin provided histopathological improvement. In the established PVR model, we showed that both doses provided biochemical and histopathological improvement, and 100-ng/μL astaxanthin provided a more effective recovery. This study shows that astaxanthin is a potential agent that can be used in the treatment and prophylaxis of PVR. More comprehensive studies are needed to demonstrate the safety and effectiveness of astaxanthin. Key Words: PVR, Astaxanthin, VEGF, TGF-ß