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鼠李素可减轻炎症并抑制大鼠碱烧伤诱导的角膜新生血管形成。

Rhamnazin attenuates inflammation and inhibits alkali burn-induced corneal neovascularization in rats.

作者信息

Yu Yao, Zhou Xue-Zhi, Ye Lei, Yuan Qing, Freeberg Shelby, Shi Ce, Zhu Pei-Wen, Bao Jing, Jiang Nan, Shao Yi

机构信息

Department of Ophthalmology, The First Affiliated Hospital of Nanchang University, Jiangxi Province Clinical Ophthalmology Institute No. 17, Yongwaizheng Street, Donghu District Nanchang 330006 Jiangxi China

Department of Endocrinology and Metabolism, The Third Hospital of Nanchang, Nanchang Key Laboratory of Diabetes Nanchang 330006 Jiangxi China.

出版信息

RSC Adv. 2018 Jul 27;8(47):26696-26706. doi: 10.1039/c8ra03159b. eCollection 2018 Jul 24.

Abstract

The purpose of our study was to determine whether rhamnazin inhibits corneal neovascularization in the rat alkali burn model, and alleviates the inflammatory response of the cornea. Rhamnazin inhibited the proliferation of HUVEC cells in a dose-dependent manner, and it also inhibited the migration and luminal formation of HUVEC cells. 20 μM rhamnazin eye drops were applied to an animal model of corneal alkali burn neovascularization 4 times a day for 14 days. The corneal neovascularization in the rhamnazin group was obviously less than that in the PBS control group. In the rhamnazin group, the inflammatory index of the cornea decreased gradually over time, whereas the inflammatory index of the PBS group decreased only slightly with time. The corneal CNV area in the PBS group was significantly larger than that in the rhamnazin group. The expression level of VEGF protein of the rhamnazin group was lower than that in the PBS group, and the expression level of PEDF was significantly higher than that of the PBS group. Rhamnazin downregulated the expression of VEGFR2 protein and decreased the expression levels of p-STAT3, p-MAPK and p-Akt proteins. This study provides a new idea for the study of the molecular mechanism of corneal neovascularization.

摘要

我们研究的目的是确定鼠李素是否能抑制大鼠碱烧伤模型中的角膜新生血管形成,并减轻角膜的炎症反应。鼠李素以剂量依赖性方式抑制人脐静脉内皮细胞(HUVEC)的增殖,还抑制HUVEC细胞的迁移和管腔形成。将20μM鼠李素滴眼液每天4次应用于角膜碱烧伤新生血管动物模型,持续14天。鼠李素组的角膜新生血管明显少于磷酸盐缓冲液(PBS)对照组。在鼠李素组中,角膜炎症指数随时间逐渐降低,而PBS组的炎症指数仅随时间略有下降。PBS组的角膜新生血管面积显著大于鼠李素组。鼠李素组血管内皮生长因子(VEGF)蛋白表达水平低于PBS组,色素上皮衍生因子(PEDF)表达水平显著高于PBS组。鼠李素下调血管内皮生长因子受体2(VEGFR2)蛋白的表达,并降低磷酸化信号转导和转录激活因子3(p-STAT3)、磷酸化丝裂原活化蛋白激酶(p-MAPK)和磷酸化蛋白激酶B(p-Akt)蛋白的表达水平。本研究为角膜新生血管形成分子机制的研究提供了新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/9083096/5757afebffe2/c8ra03159b-f1.jpg

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