Abstract

Spirulina is a type of filamentous blue-green microalgae known to be rich in nutrients and to have pharmacological effects, but the effect of spirulina on the small intestine epithelium is not well understood. Therefore, this study aims to investigate the proliferative effects of spirulina crude protein (SPCP) on a rat intestinal epithelial cells IEC-6 to elucidate the mechanisms underlying its effect. First, the results of wound-healing and cell viability assays demonstrated that SPCP promoted migration and proliferation in a dose-dependent manner. Subsequently, when the mechanisms of migration and proliferation promotion by SPCP were confirmed, we found that the epidermal growth factor receptor (EGFR) and mitogen-activated protein (MAPK) signaling pathways were activated by phosphorylation. Cell cycle progression from G0/G1 to S phase was also promoted by SPCP through upregulation of the expression levels of cyclins and cyclin-dependent kinases (Cdks), which regulate cell cycle progression to the S phase. Meanwhile, the expression of cyclin-dependent kinase inhibitors (CKIs), such as p21 and p27, decreased with SPCP. In conclusion, our results indicate that activation of EGFR and its downstream signaling pathway by SPCP treatment regulates cell cycle progression. Therefore, these results contribute to the research on the molecular mechanism for SPCP promoting the migration and proliferation of rat intestinal epithelial cells.

Highlights

  • The surface of the intestinal epithelium is covered with a monolayer of intestinal epithelial cells (IECs), which digest food, absorb nutrients and prevent harmful external agents, such as toxins, allergens, and pathogens from entering the body [1,2]

  • epidermal growth factor receptor (EGFR) demonstrated activity in regulating the migration and proliferation of IECs, and recent evidence indicates that spirulina crude protein (SPCP) increases the cellular viability of human dermal fibroblasts (CCD-986sk) by activating the EGFR/mitogen-activated protein kinase (MAPK) signaling pathway [31]. These results suggest that SPCP effectively regulates the EGFR/MAPK signaling pathway

  • In contrast the levels of p21 and p27 that inhibit cyclin-dependent kinases (Cdks) activity declined (Figure 7B). These results suggest that SPCP promotes proteins p21 and p27 that inhibit Cdk activity declined (Figure 7B)

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Summary

Introduction

The surface of the intestinal epithelium is covered with a monolayer of intestinal epithelial cells (IECs), which digest food, absorb nutrients and prevent harmful external agents, such as toxins, allergens, and pathogens from entering the body [1,2]. When the surface of the intestinal epithelium is damaged, IECs adjacent to the injured region migrate to the damaged area and proliferate through cell division to maintain homeostasis of the intestinal mucosa [4] Intestinal disorders such as inflammatory bowel disease (IBD) cause repeated damage to the intestinal mucosal surface, resulting in IEC defects [5,6,7].

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