Jolkinolide A抑制VEGF诱导的视网膜内皮细胞增殖
Jolkinolide A Blocks VEGF-Induced Proliferation in Vitro in Primary Human Retinal Microvascular Endothelial Cells
章雪敏 1王新欣 1杨军兴 1刘建亮1
作者信息
- 1. 山东第二医科大学附属医院眼科,山东潍坊 261053;山东第二医科大学临床医学院,山东潍坊 261053
- 折叠
摘要
异常血管生成与糖尿病性视网膜病变和年龄相关性黄斑变性等眼部疾病有关,目前针对这些眼部疾病的治疗方法并不令人满意.为了确定从大戟属植物中分离出的岩大戟内酯A(Jolkinolide A,JKL-A)是否能抑制血管内皮生长因子(VEGF)诱导的血管内皮细胞(HRECs)的信号转导和细胞反应,研究发现10 μmol/L的JKL-A可特异性地抑制VEGF诱导的VEGFR2的激活及其下游信号酶AKT和ERK的活性.此外,发现JKL-A能有效地增强康柏西普(conbercept)对人视网膜内皮细胞(HRECs)的细胞活力、细胞迁移和凋亡的影响.这意味着JKL-A可能是预防与治疗血管生成相关的疾病(如糖尿病性视网膜病变)的一种有前途的新药.
Abstract
Abnormal angiogenesis is associated with intraocular diseases such as proliferative diabetic retinopathy and neovascular age-related macular degeneration,and current therapies for these eye diseases are not satisfactory.The purpose of this study was to determine whether Jolkinolide A(JKL-A)isolated from Euphorbia fischeriana can inhibit vascular endothelial growth factor(VEGF)-induced angiogenesis and cellular responses in primary human retinal microvascular endothelial cells(HRECs).Our study revealed that 20 μmol/L Jolkinolide A specifically inhibited VEGF-induced activation of VEGFR2 and its downstream signaling enzymes Akt and Erk.In addition,this chemical effectively enhanced the effects of conbercept on cell viability,cell migration,and apoptosis in HRECs was found.The results suggests that JKL-A is a promising prophylactic for angiogenesis-associated diseases such as proliferative diabetic retinopathy.
关键词
Jolkinolide/A/糖尿病性视网膜病变/VEGF/细胞迁移/细胞增殖Key words
jolkinolide A/proliferative diabetic retinopathy/VEGF/cell migration/cell proliferation引用本文复制引用
出版年
2024
NETL
NSTL
万方数据