青葙苷I 通过调节ROS 介导的JNK/c-Jun 信号通路增强视神经损伤模型视网膜 神经节细胞的线粒体自噬

AIM: This study aimed to investigate the mechanism by which celoside I enhances mitophagy in a model of optic nerve injury through regulation of reactive oxygen species（ ROS）-mediated c-Jun N-terminal kinase（ JNK）/c-Jun signaling pathway. METHODS: Twenty-four New Zealand white rabbits were randomly divided into four groups: sham surgery, model, mecobalamin, and experimental group. Optic nerve injury was induced in the model, mecobalamin, and experimental groups, while the sham surgery group underwent a sham procedure. The mecobalamin group received mecobalamin, the experimental group received celoside I, and the sham surgery and model groups received saline. Interventions were administered daily for 28 d. Various techniques including endoscopy, hematoxylin-eosin （HE） staining, TUNEL method, immunofluorescence staining and Western blot were used to assess fundus condition, retinal morphology, apoptosis, ROS expression, and protein levels in the retina. RESULTS: Fundus examination revealed improved blood flow in the mecobalamin and experimental groups compared to the model group. Retinal morphology showed enhanced retinal ganglion cells （RGCs） in the mecobalamin and experimental groups. Apoptosis index was lower in the mecobalamin group compared to the experimental group. Immunofluorescence staining indicated reduced ROS and P62 expression and increased parkin and microtubule-associated protein light chain 3 （LC3） expression in the experimental group compared to the mecobalamin group. Protein analysis showed decreased JNK, c-Jun, and P62 levels, and increased parkin and LC3 levels in the mecobalamin and experimental groups compared to the model group. CONCLUSION: Celoside I reduces ROS expression, inhibits the JNK/c-Jun pathway, enhances mitophagy, reduces apoptosis, and protects RGCs in optic nerve injury models. [ABSTRACT FROM AUTHOR]