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作 者:章雪敏 王新欣 杨军兴 刘建亮 Zhang Xuemin;Wang Xinxin;Yang Junxing;Liu Jianliang(Department of O phtalmology Affiliated Hospital of Shandong Second Medical University,Weifang 261053,China;Clinical Medical College,Shandong Second Medical University,Weifang 261053,China)
机构地区:[1]山东第二医科大学附属医院眼科,山东潍坊261053 [2]山东第二医科大学临床医学院,山东潍坊261053
出 处:《南开大学学报(自然科学版)》2024年第4期86-89,共4页Journal of Nankai University(Natural Sience)
基 金:山东省医药卫生科技发展计划项目(202207020859)。
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10μmol/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.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 20μmol/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.
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