Investigative ophthalmology & visual science · 2026
Neuroprotective and Anti-Inflammatory Effects of SOCS1 Mimetic Peptides in Mouse Diabetic Retinopathy.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Salobrar-García Elena, Opazo-Ríos Lucas, Matamoros José A, Sánchez-Puebla Lidia, Fernández-Albarral José A, Salazar Juan J, Castro Raquel, Soto-Catalán Manuel, Moreno Juan Antonio, Gómez-Guerrero Carmen, Mas Sebastián, Egido Jesús, Ramírez Ana I
Аннотация
PURPOSE: To evaluate the therapeutic potential of a suppressor of cytokine signaling 1 (SOCS1) mimetic peptide (MiS1) via systemic administration in a mouse model of diabetic retinopathy (DR).
METHODS: Male db/db mice, a model of type 2 diabetes, were treated for 7 weeks with intraperitoneal injections of MiS1. In comparison, a group of animals received the Janus kinase (JAK)1/2 inhibitor baricitinib. Untreated diabetic db/db mice and non-diabetic db/m littermates served as controls. Retinal structure was assessed in vivo by optical coherence tomography. Retinal ganglion cell (RGC) survival (Brn3a+ cells) and Iba1-positive microglial activation (Iba1+ cells) were analyzed by immunohistochemistry in retinal wholemounts.
RESULTS: Untreated db/db mice exhibited retinal thinning, RGC loss, and marked Iba1+ microglial activation. Both MiS1 and baricitinib treatments significantly attenuated retinal thinning, with MiS1 preserving retinal thickness at levels comparable to those of nondiabetic controls. RGC numbers were partially preserved in both treated groups, although the increase compared with untreated db/db mice reached statistical significance only in baricitinib-treated animals. Both treatments improved microglial morphology, mainly by increasing arbor area, whereas their effects on Iba1+ cell numbers were layer and parameter dependent.
CONCLUSIONS: Systemic administration of the SOCS1 mimetic peptide MiS1 showed a consistent protective profile on retinal thickness preservation and microglial remodeling in experimental DR. These findings support SOCS1-based therapies as a promising therapeutic strategy.
METHODS: Male db/db mice, a model of type 2 diabetes, were treated for 7 weeks with intraperitoneal injections of MiS1. In comparison, a group of animals received the Janus kinase (JAK)1/2 inhibitor baricitinib. Untreated diabetic db/db mice and non-diabetic db/m littermates served as controls. Retinal structure was assessed in vivo by optical coherence tomography. Retinal ganglion cell (RGC) survival (Brn3a+ cells) and Iba1-positive microglial activation (Iba1+ cells) were analyzed by immunohistochemistry in retinal wholemounts.
RESULTS: Untreated db/db mice exhibited retinal thinning, RGC loss, and marked Iba1+ microglial activation. Both MiS1 and baricitinib treatments significantly attenuated retinal thinning, with MiS1 preserving retinal thickness at levels comparable to those of nondiabetic controls. RGC numbers were partially preserved in both treated groups, although the increase compared with untreated db/db mice reached statistical significance only in baricitinib-treated animals. Both treatments improved microglial morphology, mainly by increasing arbor area, whereas their effects on Iba1+ cell numbers were layer and parameter dependent.
CONCLUSIONS: Systemic administration of the SOCS1 mimetic peptide MiS1 showed a consistent protective profile on retinal thickness preservation and microglial remodeling in experimental DR. These findings support SOCS1-based therapies as a promising therapeutic strategy.