Tan Shu-Qiu, Geng Xue, Liu Jorn-Hon, Pan Wynn Hwai-Tzong, Wang Li-Xiang, Liu Hui-Kang, Hu Lei, Chao Hsiao-Ming
Department of Ophthalmology, Affiliated Hospital of Taishan Medical University, Taishan, Shandong, China.
Department of Pharmacology, School of Medicine, Shandong University, Jinan, Shandong, China.
BMC Complement Altern Med. 2017 Jul 14;17(1):365. doi: 10.1186/s12906-017-1857-2.
Retinal ischemia-related eye diseases result in visual dysfunction. This study investigates the protective effects and mechanisms of Xue-Fu-Zhu-Yu decoction (XFZYD) with respect to retinal ischemia.
Retinal ischemia (I) was induced in Wistar rats by a high intraocular pressure (HIOP) of 120 mmHg for 1 h, which was followed by reperfusion of the ischemic eye; the fellow untreated eye acted as a control. Electroretinogram (ERG), biochemistry and histopathology investigations were performed.
Significant ischemic changes occurred after ischemia including decreased ERG b-wave ratios, less numerous retinal ganglion cells (RGCs), reduced inner retinal thickness, fewer choline acetyltransferase (ChAT) labeled amacrine cell bodies, increased glial fibrillary acidic protein (GFAP) immunoreactivity and increased vimentin Müller immunolabeling. These were accompanied by significant increases in the mRNA/protein concentrations of vascular endothelium growth factor, hypoxia-inducible factor-1α, pyruvate kinase M2 and retinoblastoma-binding protein 2. The ischemic changes were concentration-dependently and significantly altered when XFZYD was given for seven consecutive days before or after retina ischemia, compared to vehicle. These alterations included enhanced ERG b-wave amplitudes, more numerous RGCs, enhanced inner retinal thickness, a greater number of ChAT immunolabeled amacrine cell bodies and decreased GFAP/vimentin immunoreactivity. Furthermore, decreased mRNA levels of VEGF, HIF-1α, PKM2, and RBP2 were also found. Reduced protein concentrations of VEGF, HIF-1α, PKM2, and RBP2 were also demonstrated. Furthermore, there was an inhibition of the ischemia-associated increased ratios (target protein/β-actin) in the protein levels of VEGF, HIF-1α, PKM2, and RBP2, which were induced by Shikonin, JIB-04 or Avastin.
XFZYD would seem to protect against well-known retinal ischemic changes via a synergistic inhibition of RBP2 and PKM2, as well as down-regulation of HIF-1α and a reduction in VEGF secretion.
视网膜缺血相关眼病会导致视觉功能障碍。本研究探讨血府逐瘀汤（XFZYD）对视网膜缺血的保护作用及其机制。
通过120mmHg的高眼压（HIOP）持续1小时诱导Wistar大鼠视网膜缺血（I），随后对缺血眼进行再灌注；未处理的对侧眼作为对照。进行了视网膜电图（ERG）、生化和组织病理学研究。
缺血后出现明显的缺血性变化，包括ERG b波比值降低、视网膜神经节细胞（RGC）数量减少、视网膜内层厚度变薄、胆碱乙酰转移酶（ChAT）标记的无长突细胞体数量减少、胶质纤维酸性蛋白（GFAP）免疫反应性增加和波形蛋白穆勒免疫标记增加。这些变化伴随着血管内皮生长因子、缺氧诱导因子-1α、丙酮酸激酶M2和视网膜母细胞瘤结合蛋白2的mRNA/蛋白浓度显著增加。与赋形剂相比，在视网膜缺血前或后连续7天给予XFZYD时，缺血性变化呈浓度依赖性且显著改变。这些改变包括增强的ERG b波振幅、更多的RGC、增强的视网膜内层厚度、更多的ChAT免疫标记的无长突细胞体以及降低的GFAP/波形蛋白免疫反应性。此外，还发现VEGF、HIF-1α、PKM2和RBP2的mRNA水平降低。VEGF、HIF-1α、PKM2和RBP2的蛋白浓度也降低。此外，还抑制了由紫草素、JIB-04或阿瓦斯汀诱导的VEGF、HIF-1α、PKM2和RBP2蛋白水平的缺血相关增加比率（靶蛋白/β-肌动蛋白）。
血府逐瘀汤似乎通过协同抑制RBP2和PKM2，以及下调HIF-1α和减少VEGF分泌来预防众所周知的视网膜缺血性变化。
Zotero 插件