스피루리나 단백질에 의한 소장 상피세포의 증식 촉진 메커니즘

Abstract

The surface of the intestinal tract is covered with a monolayer of intestinal epithelial cells (IECs), which serves as a barrier to external substances, microbes, and viruses. The loss of IECs is known to be a major contributor to inflammatory bowel disease. When the intestinal mucosa is damaged, epithelial cell proliferation is required for recovery. After damage, IECs migrate to the affected area and restore the intestinal mucosa by proliferation through cell division. Spirulina is a type of filamentous blue-green algae known to contain various nutrients, especially C-phycocyanin; however, the effect of spirulina on the small intestine epithelium is not well understood. Therefore, this study aims to investigate the proliferative effects of protein (SPCP) on IEC-6 cells and elucidate the underlying mechanisms. First, a cell viability assay and wound healing assay demonstrated that SPCP induced cell proliferation and migration in a dose-dependent manner. Subsequently, this examined the mechanisms for proliferation induced by SPCP. This study found that epidermal growth factor receptor (EGFR) stimulated the proliferation of IECs, and SPCP induced an increase in the phosphorylation of EGFR. Additionally, the activation of EGFR stimulated the MAPK/ERK pathway and the PI3K/Akt/mTOR pathway for cell growth, proliferation, and survival. Flow cytometry results showed cell cycle progression from the G1 to the S phase after SPCP treatment. This G1 to S phase transition was promoted by SPCP by upregulating the expression levels of cyclins and cyclin-dependent kinases (Cdks), which regulate cell cycle progression to the S phase. Also, the expression of cyclin-dependent kinase inhibitors (CKIs) such as p21 and p27 was decreased by SPCP. These results indicate that the activation of EGFR and its downstream signaling pathway by SPCP treatment regulated cell cycle progression in intestinal epithelial cells. Therefore, SPCP could potentially be consumed as a functional food to increase the proliferation of intestinal epithelial cells.