大黄素通过血管内皮生长因子受体2信号通路抑制碱烧伤诱导的角膜炎症和新生血管。

Zheng Xueying, Guo Liang, Lai Siyi, L I Fengyue, Liang Mingli, Liu Wanting, Meng Chun, Liu Guanghui
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引用次数: 0

摘要

目的:研究大黄素对碱灼伤引起的角膜炎症和新生血管的影响:研究大黄素对碱烧伤诱导的角膜炎症和新生血管的影响:方法:通过分子对接预测大黄素靶向血管内皮生长因子受体2(VEGFR2)的能力。大黄素对人脐静脉内皮细胞(HUVEC)侵袭、迁移和增殖的影响是通过细胞计数试剂盒-8、Transwell和管形成试验测定的。细胞凋亡分析采用流式细胞术进行。用免疫荧光法检测 CD31 水平。通过免疫印迹分析检测血管内皮生长因子受体2(VEGFR2)、蛋白激酶B(Akt)、信号转导及转录激活因子3(STAT3)和P38的丰度和磷酸化状态。对 40 只小鼠进行角膜碱烧伤。将小鼠随机分为两组,然后用 10 μM 大黄素或磷酸盐缓冲盐水(PBS)滴眼液治疗碱烧伤的眼睛,每天四次。在第 0、7、10 和 14 天,用裂隙灯显微镜评估所有眼睛的炎症和角膜新生血管(CNV)情况。碱烧伤14天后,小鼠被人道处死,角膜被取出并保存在-80 ℃下,直至组织学研究或蛋白质提取:结果:分子对接证实大黄素能靶向血管内皮生长因子受体2。结果:分子对接证实大黄素能靶向血管内皮生长因子受体 2(VEGFR2),并发现大黄素能以剂量依赖的方式减少 HUVEC 的侵袭、迁移、血管生成和增殖。在小鼠中,大黄素能抑制角膜炎症细胞浸润,抑制碱烧伤诱导的角膜新生血管的发展。与 PBS 处理组相比,大黄素处理组的 VEGFR2 表达和 CD31 水平较低。大黄素显著降低了VEGF处理的HUVEC中VEGFR2、p-VEGFR2、p-Akt、p-STAT3和p-P38的表达:这项研究为评估角膜炎症和新生血管形成的分子机制提供了一条新途径。大黄素可能是治疗角膜碱烧伤的一种很有前景的新疗法。
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Emodin suppresses alkali burn-induced corneal inflammation and neovascularization by the vascular endothelial growth factor receptor 2 signaling pathway.

Objective: To investigate the effects of emodin on alkali burn-induced corneal inflammation and neovascularization.

Methods: The ability of emodin to target vascular endothelial growth factor receptor 2 (VEGFR2) was predicted by molecular docking. The effects of emodin on the invasion, migration, and proliferation of human umbilical vein endothelial cells (HUVEC) were determined by cell counting kit-8, Transwell, and tube formation assays. Analysis of apoptosis was performed by flow cytometry. CD31 levels were examined by immunofluorescence. The abundance and phosphorylation state of VEGFR2, protein kinase B (Akt), signal transducer and activator of transcription 3 (STAT3), and P38 were examined by immunoblot analysis. Corneal alkali burn was performed on 40 mice. Animals were divided randomly into two groups, and the alkali-burned eyes were then treated with drops of either 10 μM emodin or phosphate buffered saline (PBS) four times a day. Slit-lamp microscopy was used to evaluate inflammation and corneal neovascularization (CNV) in all eyes on Days 0, 7, 10, and 14. The mice were killed humanely 14 d after the alkali burn, and their corneas were removed and preserved at -80 ℃ until histological study or protein extraction.

Results: Molecular docking confirmed that emodin was able to target VEGFR2. The findings revealed that emodin decreased the invasion, migration, angiogenesis, and proliferation of HUVEC in a dose-dependent manner. In mice, emodin suppressed corneal inflammatory cell infiltration and inhibited the development of corneal neovascularization induced by alkali burn. Compared to those of the PBS-treated group, lower VEGFR2 expression and CD31 levels were found in the emodin-treated group. Emodin dramatically decreased the expression of VEGFR2, p-VEGFR2, p-Akt, p-STAT3, and p-P38 in VEGF-treated HUVEC.

Conclusion: This study provides a new avenue for evaluating the molecular mechanisms underlying corneal inflammation and neovascularization. Emodin might be a promising new therapeutic option for corneal alkali burns.

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