PDF(Pubmed)
Abstract：
UNASSIGNED: The study aims to investigate the protective effect of Mingjing granule (MG) in a fibrovascular membrane rat model of neovascular age-related macular degeneration (nAMD) and explore the underlying mechanism.
UNASSIGNED: The nAMD fibrovascular membrane model was established by two-stage laser photocoagulation. BN rats were randomly divided into four groups: the model group was gavaged with distilled water, the anti-VEGF group was given an intravitreous injection of ranibizumab, the MG + anti-VEGF group was gavaged with MG combined with an intravitreous injection of ranibizumab, and the normal group not modeled only fed conventionally. Lesions were evaluated by color fundus photograph, optical coherence tomography, fundus fluorescein angiography, and retinal pigment epithelial-choroid-sclera flat mount. The changes in the retinal structure were observed by histopathology. The expression of inflammatory cell markers F4/80, Iba-1, and glial fibrillary acidic protein (GFAP); the fibrosis-related factors collagen-1, fibronectin, α-smooth muscle actin (α-SMA), and transforming growth factor-beta (TGF-β); and the complement system-related factors C3a and C3aR in the retina were detected by immunofluorescence or qRT-PCR.
UNASSIGNED: The current study revealed that MG + anti-VEGF administration more significantly reduced the thickness of fibrovascular lesions, suppressed vascular leakage (exudation area and mean density value), inhibited the area of fibrovascular lesions, and restrained the formation of the fibrovascular membrane than the anti-VEGF agent alone in the two-stage laser-induced rat model. The fluorescence intensities of F4/80, Iba-1, collagen-1, fibronectin, TGF-β, and C3aR showed more significant inhibition in MG + anti-VEGF-treated rats than the anti-VEGF agent alone. The mRNA expression levels of F4/80, Iba-1, GFAP, collagen-1, fibronectin, α-SMA, TGF-β, and C3a showed lower levels in rats treated with MG + anti-VEGF than the anti-VEGF agent alone.
UNASSIGNED: Combining MG with anti-VEGF treatment inhibits the growth of the fibrovascular membrane more effectively than using anti-VEGF treatment alone. The mechanism underlying this effect may involve limiting inflammatory cell aggregation, controlling complement system activation, and decreasing the expression of the fibrotic protein.
UNASSIGNED: The nAMD fibrovascular membrane model was established by two-stage laser photocoagulation. BN rats were randomly divided into four groups: the model group was gavaged with distilled water, the anti-VEGF group was given an intravitreous injection of ranibizumab, the MG + anti-VEGF group was gavaged with MG combined with an intravitreous injection of ranibizumab, and the normal group not modeled only fed conventionally. Lesions were evaluated by color fundus photograph, optical coherence tomography, fundus fluorescein angiography, and retinal pigment epithelial-choroid-sclera flat mount. The changes in the retinal structure were observed by histopathology. The expression of inflammatory cell markers F4/80, Iba-1, and glial fibrillary acidic protein (GFAP); the fibrosis-related factors collagen-1, fibronectin, α-smooth muscle actin (α-SMA), and transforming growth factor-beta (TGF-β); and the complement system-related factors C3a and C3aR in the retina were detected by immunofluorescence or qRT-PCR.
UNASSIGNED: The current study revealed that MG + anti-VEGF administration more significantly reduced the thickness of fibrovascular lesions, suppressed vascular leakage (exudation area and mean density value), inhibited the area of fibrovascular lesions, and restrained the formation of the fibrovascular membrane than the anti-VEGF agent alone in the two-stage laser-induced rat model. The fluorescence intensities of F4/80, Iba-1, collagen-1, fibronectin, TGF-β, and C3aR showed more significant inhibition in MG + anti-VEGF-treated rats than the anti-VEGF agent alone. The mRNA expression levels of F4/80, Iba-1, GFAP, collagen-1, fibronectin, α-SMA, TGF-β, and C3a showed lower levels in rats treated with MG + anti-VEGF than the anti-VEGF agent alone.
UNASSIGNED: Combining MG with anti-VEGF treatment inhibits the growth of the fibrovascular membrane more effectively than using anti-VEGF treatment alone. The mechanism underlying this effect may involve limiting inflammatory cell aggregation, controlling complement system activation, and decreasing the expression of the fibrotic protein.
摘要：
■本研究旨在研究明精颗粒（MG）对新生血管性年龄相关性黄斑变性（nAMD）大鼠血管膜模型的保护作用，并探讨其机制。
■通过两级激光光凝法建立nAMD纤维血管膜模型。将BN大鼠随机分为4组:模型组给予蒸馏水灌胃,抗VEGF组给予雷珠单抗玻璃体内注射,MG+抗VEGF组接受MG联合雷珠单抗玻璃体内注射，正常组不是只按常规喂养的模型。通过彩色眼底照片评估病变，光学相干层析成像，荧光素眼底血管造影,和视网膜色素上皮-脉络膜-巩膜平坦安装。通过组织病理学观察视网膜结构的变化。炎症细胞标志物F4/80、Iba-1和胶质纤维酸性蛋白(GFAP)的表达;纤维化相关因子α-平滑肌肌动蛋白（α-SMA），和转化生长因子-β（TGF-β）；通过免疫荧光或qRT-PCR检测视网膜中补体系统相关因子C3a和C3aR。
■目前的研究表明，MG+抗VEGF给药更显著地降低了纤维血管病变的厚度，抑制血管渗漏（渗出面积和平均密度值），抑制了纤维血管病变的区域，在两阶段激光诱导的大鼠模型中，与单独的抗VEGF剂相比，抑制了纤维血管膜的形成。F4/80、Iba-1、胶原-1、纤连蛋白的荧光强度,TGF-β,和C3aR在MG+抗VEGF治疗的大鼠中显示出比单独的抗VEGF剂更显著的抑制。F4/80，Iba-1，GFAP的mRNA表达水平，胶原-1，纤连蛋白，α-SMA,TGF-β,和C3a在用MG+抗VEGF治疗的大鼠中显示出比单独的抗VEGF药物更低的水平。
■与单独使用抗VEGF治疗相比，将MG与抗VEGF治疗组合更有效地抑制纤维血管膜的生长。这种效应的潜在机制可能涉及限制炎症细胞聚集，控制补体系统激活，并降低纤维化蛋白的表达。
■通过两级激光光凝法建立nAMD纤维血管膜模型。将BN大鼠随机分为4组:模型组给予蒸馏水灌胃,抗VEGF组给予雷珠单抗玻璃体内注射,MG+抗VEGF组接受MG联合雷珠单抗玻璃体内注射，正常组不是只按常规喂养的模型。通过彩色眼底照片评估病变，光学相干层析成像，荧光素眼底血管造影,和视网膜色素上皮-脉络膜-巩膜平坦安装。通过组织病理学观察视网膜结构的变化。炎症细胞标志物F4/80、Iba-1和胶质纤维酸性蛋白(GFAP)的表达;纤维化相关因子α-平滑肌肌动蛋白（α-SMA），和转化生长因子-β（TGF-β）；通过免疫荧光或qRT-PCR检测视网膜中补体系统相关因子C3a和C3aR。
■目前的研究表明，MG+抗VEGF给药更显著地降低了纤维血管病变的厚度，抑制血管渗漏（渗出面积和平均密度值），抑制了纤维血管病变的区域，在两阶段激光诱导的大鼠模型中，与单独的抗VEGF剂相比，抑制了纤维血管膜的形成。F4/80、Iba-1、胶原-1、纤连蛋白的荧光强度,TGF-β,和C3aR在MG+抗VEGF治疗的大鼠中显示出比单独的抗VEGF剂更显著的抑制。F4/80，Iba-1，GFAP的mRNA表达水平，胶原-1，纤连蛋白，α-SMA,TGF-β,和C3a在用MG+抗VEGF治疗的大鼠中显示出比单独的抗VEGF药物更低的水平。
■与单独使用抗VEGF治疗相比，将MG与抗VEGF治疗组合更有效地抑制纤维血管膜的生长。这种效应的潜在机制可能涉及限制炎症细胞聚集，控制补体系统激活，并降低纤维化蛋白的表达。
