Abstract：
In this study, N-Methyl-N-nitrosourea (MNU) was intraperitoneally injected to construct a mouse retinitis pigmentosa (RP) model to evaluate the protective effect of chitosan and β-carotene on RP. The results demonstrated that chitosan synergized with β-carotene significantly reduced retinal histopathological structural damage in RP mice. The co-treatment group of β-carotene and chitosan restored the retinal thickness and outer nuclear layer thickness better than the group treated with the two alone, and the thickness reached the normal level. The content of β-carotene and retinoids in the liver of chitosan and β-carotene co-treated group increased by 46.75 % and 20.69 %, respectively, compared to the β-carotene group. Chitosan and β-carotene supplement suppressed the expressions of Bax, Calpain2, Caspase3, NF-κB, TNF-α, IL-6, and IL-1β, and promoted the up-regulation of Bcl2. Chitosan and β-carotene interventions remarkably contributed to the content of SCFAs and enhanced the abundance of Ruminococcaceae, Rikenellaceae, Odoribacteraceae and Helicobacteraceae. Correlation analysis demonstrated a strong association between gut microbiota and improvement in retinitis pigmentosa. This study will provide a reference for the study of the gut-eye axis.
摘要：
在这项研究中,腹腔注射N-甲基-N-亚硝基脲(MNU)构建小鼠视网膜色素变性(RP)模型,评价壳聚糖和β-胡萝卜素对RP的保护作用。结果表明，壳聚糖与β-胡萝卜素协同作用可显著降低RP小鼠视网膜组织病理学结构损伤。β-胡萝卜素和壳聚糖联合治疗组视网膜厚度和外核层厚度的恢复优于单独治疗组,厚度达到正常水平。壳聚糖和β-胡萝卜素共处理组肝脏中β-胡萝卜素和类维生素A的含量分别增加了46.75%和20.69%,分别,与β-胡萝卜素组相比。壳聚糖和β-胡萝卜素的补充抑制Bax的表达，Calpain2,Caspase3,NF-κB,TNF-α,IL-6和IL-1β，并促进了Bcl2的上调。壳聚糖和β-胡萝卜素干预显着促进了SCFA的含量，并增强了Ruminococycaceae的丰度，Rikenellaceae，恶杆菌科和螺旋杆菌科。相关分析表明肠道菌群与色素性视网膜炎的改善之间存在很强的关联。本研究将为肠眼轴的研究提供参考。
