首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Extract of the Blood Circulation-Promoting Recipe-84 Can Protect Rat Retinas by Inhibiting the β-Catenin Signaling Pathway
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Extract of the Blood Circulation-Promoting Recipe-84 Can Protect Rat Retinas by Inhibiting the β-Catenin Signaling Pathway

机译:血液循环促进食谱84的提取物可以通过抑制β-连环蛋白信号通路来保护大鼠视网膜

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摘要

Extract of the Blood Circulation-Promoting Recipe (EBR-84) from the Chinese Herbal medicine “Blood Circulation Promoting Recipe” could retard retinopathy development. This study investigated whether EBR-84 protects retinas by inhibiting the β-catenin pathway using a rat model of retinopathy and a retinal ganglion cell 5 (RGC-5) cell death model. RGC death was induced by either N-methyl-d-aspartic acid (NMDA) or TWS119 (an activator of the β-catenin pathway). After the corresponding treatment with EBR-84, RGC death and the protein expression levels of β-catenin, cyclooxygenase-2 (COX-2), and vascular endothelial growth factor (VEGF) in rat retinas were examined. β-Catenin accumulated in the retinal ganglion cell layer (GCL) of NMDA-treated rats. EBR-84 (3.9, 7.8, and 15.6 g/kg) significantly attenuated the NMDA-induced RGC loss accompanying the reduction of β-catenin expression. Moreover, the expression levels of COX-2 and VEGF were decreased by EBR-84 in a dose-dependent manner. For the TWS119-treated rats, EBR-84 also ameliorated RGC loss and lowered the expression levels of β-catenin, COX-2, and VEGF. In vitro, EBR-84 increased the viability of NMDA-treated RGC-5 while decreased β-catenin expression. In conclusion, EBR-84 retarded ratretinopathy, and the β-catenin signaling pathway played an important role during this protective process.
机译:从中药“活血化瘀方”中提取活血化瘀方(EBR-84)可延缓视网膜病变的发展。这项研究使用大鼠视网膜病变模型和视网膜神经节细胞5(RGC-5)细胞死亡模型研究了EBR-84是否通过抑制β-catenin途径来保护视网膜。 RGC死亡是由N-甲基-d-天冬氨酸(NMDA)或TWS119(β-连环蛋白途径的激活剂)诱导的。在用EBR-84进行相应处理后,检查了大鼠视网膜中RGC的死亡以及β-catenin,环氧合酶2(COX-2)和血管内皮生长因子(VEGF)的蛋白表达水平。 β-连环蛋白累积在NMDA处理的大鼠的视网膜神经节细胞层(GCL)中。 EBR-84(3.9、7.8和15.6 g / kg)显着减轻了NMDA诱导的RGC损失,伴随着β-catenin表达的降低。此外,EBR-84以剂量依赖的方式降低了COX-2和VEGF的表达水平。对于TWS119治疗的大鼠,EBR-84还改善了RGC的丢失并降低了β-catenin,COX-2和VEGF的表达水平。在体外,EBR-84增加了NMDA处理的RGC-5的活力,同时降低了β-连环蛋白的表达。总之,EBR-84抑制了大鼠视网膜病变,β-catenin信号通路在该保护过程中发挥了重要作用。

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