Wu Bin, Wang Xue, Zhang Wei, Wang Xin, Wang Qi-Miao, Pang Ya-Ju, Kong Yi-Chun
Tianjin Eye Hospital, Tianjin Key Lab of Ophthalmology and Visual Science, Tianjin Eye Institute, Clinical College of Ophthalmology Tianjin Medical University, Tianjin 300102, China.
Department of Ophthalmology, Tianjin Hospital of Integrated Traditional Chinese and Western Medicine, Tianjin 300100, China.
Int J Ophthalmol. 2025 Feb 18;18(2):216-221. doi: 10.18240/ijo.2025.02.03. eCollection 2025.
To explore the effect and mechanism of polysaccharide (LBP) inhibiting retinal neovascularization.
tests were performed on human retinal microvascular endothelial cells (HRECs) from three groups, including control group (normal oxygen), hypoxic group (hypoxia at 37°C, 1% O, 5% CO, and 94% N), and LBP group (hypoxic group with LBP 100 µg/mL). experiments, C57 mice were divided into three groups: control group (normal rearing group), the oxygen-induced ischemic retinopathy (OIR) group, and the OIR with 50 mg/kg LBP group. Retinal neovascularization was observed by fluorescein angiography and quantified. Retinal thickness was evaluated by Hematoxylin and eosin (HE) stain. The expression of epidermal growth factor receptor (EGFR), phosphatidylinositol 3-kinase (PI3K), mammalian target of rapamycin (mTOR), phosphorylated mammalian target of rapamycin (p-mTOR), protein kinase B (AKT), phosphorylated protein kinase B (p-AKT), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF-α) in each group were analyzed by Western blot. IL-1β level in retina was analyzed using immunohistochemical staining.
The increased area of neovascular clusters in OIR mice was significantly decreased by LBP. Retinal thickness of OIR mice was significantly thinner compared with normal oxygenated mice and was increased in LBP group. Compared with those in the hypoxic groups, Western blotting of HRECs and retinal tissues revealed that the expression of EGFR, PI3K, p-mTOR, p-AKT, IL-1β, iNOS, and TNF-α decreased in the LBP group but was still greater than that in control group. Moreover, IL-1β was reduced in retinal sections treated with LBP. In the scratch test, the cell migration of the hypoxic group was significantly greater than that of the control group, while LBP treatment attenuated this increase in migration.
LBP reduces retinal neovascularization and inflammation and inhibits the migration of HRECs by regulating the EGFR/PI3K/Akt/mTOR signaling pathway.
探讨枸杞多糖（LBP）抑制视网膜新生血管形成的作用及机制。
对三组人视网膜微血管内皮细胞（HRECs）进行检测，包括对照组（常氧）、低氧组（37℃、1%O₂、5%CO₂和94%N₂条件下低氧）和LBP组（低氧组+100μg/mL LBP）。实验中，将C57小鼠分为三组：对照组（正常饲养组）、氧诱导缺血性视网膜病变（OIR）组和50mg/kg LBP的OIR组。通过荧光素血管造影观察并量化视网膜新生血管形成。用苏木精-伊红（HE）染色评估视网膜厚度。采用蛋白质免疫印迹法分析各组中表皮生长因子受体（EGFR）、磷脂酰肌醇3-激酶（PI3K）、雷帕霉素靶蛋白（mTOR）、磷酸化雷帕霉素靶蛋白（p-mTOR）、蛋白激酶B（AKT）、磷酸化蛋白激酶B（p-AKT）、白细胞介素-1β（IL-1β）、诱导型一氧化氮合酶（iNOS）和肿瘤坏死因子-α（TNF-α）的表达。用免疫组织化学染色分析视网膜中IL-1β水平。
LBP显著降低了OIR小鼠新生血管簇的增加面积。与常氧小鼠相比，OIR小鼠的视网膜厚度显著变薄，而LBP组有所增加。与低氧组相比，HRECs和视网膜组织的蛋白质免疫印迹显示，LBP组中EGFR、PI3K、p-mTOR、p-AKT、IL-1β、iNOS和TNF-α的表达降低，但仍高于对照组。此外，LBP处理的视网膜切片中IL-1β减少。在划痕试验中，低氧组的细胞迁移明显大于对照组，而LBP处理减弱了这种迁移增加。
LBP通过调节EGFR/PI3K/Akt/mTOR信号通路减少视网膜新生血管形成和炎症，并抑制HRECs的迁移。
