Article

Apigenin modulates the expression levels of pro-inflammatory mediators to reduce the human insulin amyloid-induced oxidant damages in SK-N-MC cells R Amini1, R Yazdanparast1 and SH Ghaffari2 Amyloid depositions of proteins play crucial roles in a wide variety of degenerative disorders called amyloido-sis. Although the exact mechanisms involved in amyloid-mediated cytotoxicity remain unknown, increased for-mation of reactive oxygen species (ROS) and nitrogen species and overproduction of pro-inflammatory cytokines are believed to play key roles in the process. In that regard, we investigated the effect of apigenin, a common dietary flavonoid with high antioxidant and anti-inflammatory properties on potential factors involved in cytotoxicity of human insulin amyloids. Pretreatment of SK-N-MC neuroblastoma cells with api-genin increased cell viability and reduced the apoptosis induced by insulin fibrils. In addition, apigenin attenu-ated insulin fibril-induced ROS production and lipid peroxidation. Our result also demonstrated that pretreatment of the fibril-affected cells with apigenin caused an increase in catalase activity and the intracellular glutathione content along with reduction in nitric oxide production and nuclear factor B, tumor necrosis fac-tor a, and interleukin 6 gene expression based on real-time polymerase chain reaction evaluation. In accor-dance with these results, apigenin could be a promising candidate in the design of natural-based drugs for treatment or prevention of amyloid-related disorders