Bashllari Romina, Molonia Maria Sofia, Muscarà Claudia, Speciale Antonio, Wilde Peter J, Saija Antonella, Cimino Francesco
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
"Prof. Antonio Imbesi" Foundation, University of Messina, Messina, Italy.
Arch Physiol Biochem. 2023 Apr;129(2):379-386. doi: 10.1080/13813455.2020.1828480. Epub 2020 Oct 6.
Increased free fatty acids (FFAs) levels, typical in obesity condition, can contribute to systemic lipotoxicity and inflammation adversely influencing Inflammatory Bowel Disease development and progression. Anthocyanins possess health promoting properties mainly associated to the induction of Nrf2-regulated cytoprotective proteins.
Using a novel experimental model, we evaluated the in vitro intracellular mechanisms involved in FFAs modulation of intestinal epithelial lipotoxicity and the protective effects of cyanidin-3-O-glucoside (C3G) in Caco-2 cells.
Caco-2 exposed to palmitic acid (PA) in the serosal (basolateral) side showed a combined state of epithelial inflammation, inducing NF-κB pathway and downstream cytokines, that was reverted by C3G apical pre-treatment. In addition, PA altered intracellular redox status and induced reactive oxygen species that were reduced by C3G via the redox-sensitive Nrf2 signalling.
Results suggest that anti-inflammatory properties of anthocyanins, mediated by Nrf2, could represent an interesting tool for intestinal inflammatory disorders.
肥胖状态下典型的游离脂肪酸(FFA)水平升高可导致全身脂毒性和炎症,对炎症性肠病的发生和发展产生不利影响。花青素具有促进健康的特性,主要与诱导Nrf2调节的细胞保护蛋白有关。
使用一种新型实验模型,我们评估了FFA调节肠上皮脂毒性的体外细胞内机制以及花青素-3-O-葡萄糖苷(C3G)对Caco-2细胞的保护作用。
在浆膜(基底外侧)侧暴露于棕榈酸(PA)的Caco-2细胞表现出上皮炎症的综合状态,诱导NF-κB途径和下游细胞因子,而C3G顶端预处理可逆转这种状态。此外,PA改变了细胞内氧化还原状态并诱导了活性氧,而C3G通过氧化还原敏感的Nrf2信号传导降低了活性氧。
结果表明,由Nrf2介导的花青素的抗炎特性可能是治疗肠道炎症性疾病的一个有趣工具。