Current eye research · 2026
Eriocitrin Alleviates Choroidal Neovascularization by Promoting the Activities of Mitogen-Activated Protein Kinase Phosphatase-1 In Vivo and In Vitro.
СтатьяНазвание и аннотация: Перевод в очереди
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Zan Yue, Wang Xiaona, Xiao Xuefeng, Jia Zhi, Zhang Yuting, Zhu Manhui, Hao Gang
Аннотация
PURPOSE: Choroidal neovascularization causes vision loss, necessitating the development of novel therapeutic methods. This study examines the role of eriocitrin, a flavonoid, in choroidal neovascularization and its potential mechanism of action.
METHODS: A murine laser-induced choroidal neovascularization model and hypoxia-exposed human choroidal endothelial cells were employed. In vivo, eriocitrin or the anti-vascular endothelial growth factor agent conbercept was administered via intravitreal injection. Fundus fluorescein angiography, indocyanine green angiography, and immunofluorescent staining were used to assess choroidal neovascularization. In vitro, human choroidal endothelial cells were treated with eriocitrin under hypoxic conditions. Cell proliferation, migration, and tube formation were evaluated using 5-ethynyl-2'-deoxyuridine, Transwell, and tube formation assays. Protein levels of mitogen-activated protein kinase phosphatase-1, p-p38, and p-JNK were detected by Western blot.
RESULTS: Eriocitrin significantly attenuated choroidal neovascularization development and vascular leakage in mice in a dose-dependent manner, with a 4 µg dose showing efficacy comparable to conbercept. In hypoxic human choroidal endothelial cells, eriocitrin inhibited proliferation, migration, and tube formation. Under hypoxic conditions, eriocitrin elevated mitogen-activated protein kinase phosphatase-1 protein levels and reduced p-p38 and p-JNK expression. Inhibition of mitogen-activated protein kinase phosphatase-1 diminished the suppressive effects of eriocitrin on hypoxia-induced pro-angiogenic activities.
CONCLUSION: Eriocitrin alleviates choroidal neovascularization by promoting mitogen-activated protein kinase phosphatase-1 activity in choroidal endothelial cells, thereby inhibiting the p38 and JNK signaling pathways. These findings suggest eriocitrin as a potential therapeutic agent for choroidal neovascularization.
METHODS: A murine laser-induced choroidal neovascularization model and hypoxia-exposed human choroidal endothelial cells were employed. In vivo, eriocitrin or the anti-vascular endothelial growth factor agent conbercept was administered via intravitreal injection. Fundus fluorescein angiography, indocyanine green angiography, and immunofluorescent staining were used to assess choroidal neovascularization. In vitro, human choroidal endothelial cells were treated with eriocitrin under hypoxic conditions. Cell proliferation, migration, and tube formation were evaluated using 5-ethynyl-2'-deoxyuridine, Transwell, and tube formation assays. Protein levels of mitogen-activated protein kinase phosphatase-1, p-p38, and p-JNK were detected by Western blot.
RESULTS: Eriocitrin significantly attenuated choroidal neovascularization development and vascular leakage in mice in a dose-dependent manner, with a 4 µg dose showing efficacy comparable to conbercept. In hypoxic human choroidal endothelial cells, eriocitrin inhibited proliferation, migration, and tube formation. Under hypoxic conditions, eriocitrin elevated mitogen-activated protein kinase phosphatase-1 protein levels and reduced p-p38 and p-JNK expression. Inhibition of mitogen-activated protein kinase phosphatase-1 diminished the suppressive effects of eriocitrin on hypoxia-induced pro-angiogenic activities.
CONCLUSION: Eriocitrin alleviates choroidal neovascularization by promoting mitogen-activated protein kinase phosphatase-1 activity in choroidal endothelial cells, thereby inhibiting the p38 and JNK signaling pathways. These findings suggest eriocitrin as a potential therapeutic agent for choroidal neovascularization.