正二十八烷醇抑制DSS诱导的小鼠结肠炎症及其分子机理

摘要

With 3.0% dextran sulphate sodium salt(DSS) as inducer,ulcerativecolitis(UC) model in ICR mice was used to evaluate the anti–inflammatory effect and molecular mechanismofoctacosanol. The results showed that the health statusof mice fromoctacosanol group was improved significantly, and DAI and injureof pathological tissues were reduced. Octacosanol also improved inflammation related biochemical indices. RT–PCR was used to detect mRNA expression levelsof inflammatory factors andoctacosanolcould significantly inhibit TNF–α,IL–1β,IL–6 and iNOS gene expression. Western blotting analysis furtherconfirmed thatoctacosanol decreased the protein expressionof pro–inflammatory factors incolonic tissues.%以3%葡聚糖硫酸钠（DSS）为诱导剂，建立ICR小鼠结肠炎症模型，评估二十八烷醇的抗炎功效与分子机理。结果发现：二十八烷醇能显著改善结肠炎症小鼠的健康状况，减少DAI评分，减轻病理组织的损伤，改善炎症相关生化指标。RT–qPCR分析发现，二十八烷醇可使结肠组织前体炎症因子TNF–α、IL–1β、IL–6和iNOS等基因mRNA表达水平降低，Western blot分析进一步证实了二十八烷醇抑制炎症因子蛋白表达水平的功效。