医学
视网膜
糖尿病性视网膜病变
血管通透性
神经节细胞层
血管内皮生长因子
视网膜
血管抑制剂
标记法
眼科
病理
神经保护
视网膜电图
细胞凋亡
药理学
免疫组织化学
内科学
内分泌学
糖尿病
化学
生物
贝伐单抗
神经科学
化疗
血管内皮生长因子受体
生物化学
作者
Xiaoyu Xu,Mengchen Wang,Shuxia Zhang,Jing Wang,Xinxin Li,Xiaohui Ma,Yun Luo,Xiaobo Sun
标识
DOI:10.3389/fphar.2024.1294620
摘要
Introduction: Diabetic retinopathy (DR) represents a major cause of adult blindness, and early discovery has led to significant increase in the number of patients with DR. The drugs currently used for treatment, such as ranibizumab, mainly focus on the middle and late periods of DR, and thus do not meet the clinical need. Here, the potential mechanisms by which compound Danshen Dripping Pills (CDDP) might protect against early DR were investigated. Methods: Db/db mice were used to establish a DR model. The initial weights and HbA1c levels of the mice were monitored, and retinal pathology was assessed by hematoxylin-eosin (HE) staining. The vascular permeability of the retina and thickness of each retinal layer were measured, and electroretinogram were performed together with fundus fluorescein angiography and optical coherence tomography. The levels of inflammatory factors were examined in retinal tissue, as well as those of intercellular adhesion molecule 1 (ICAM-1), IL-6, and monocyte chemoattractant protein 1 (MCP-1) in the serum using ELISA. Immunohistochemistry was used to evaluate levels of vascular endothelial growth factor (VEGF), B-cell lymphoma 2 (Bcl-2), and Bclassociated X protein (Bax). Retinal cell injury and apoptosis were examined by TdT-mediated dUTP Nick End Labeling (TUNEL) assays. Results: The data showed that CDDP significantly improved cellular disarrangement. Imaging data indicated that CDDP could reduce vascular permeability and the amplitude of oscillatory potentials (OPs), and restore the thickness of the ganglion cell layer. Moreover, CDDP reduced the expression levels of inflammatory factors in both the retina and serum. Conclusion: These findings strongly suggest that CDDP prevents early DR through vascular and neuroprotection.
科研通智能强力驱动
Strongly Powered by AbleSci AI