Hematopoietic stem and progenitor cells (HSPCs) could be differentiated into mature myeloid and lymphoid cells, maintaining the requirements of immune cells. Atherosclerosis and ulcerative colitis (UC) drive HSPC homeostasis destruction, which triggers expansive HSPC proliferation and Ly6Chi monocyte production, contributing to aggravated inflammation. Vitisin A belongs to the anthocyanin derivatives with excellent stability and bioactivity in vitro. However, there is no report about the anti-inflammation of Vitisin A via reprogramming HSPC differentiation toward monocytes. In this study, we found that Vitisin A presents anti-inflammatory ability during the development of atherosclerosis and UC by depressing Ly6Chi monocyte production from bone marrow. This performance depended on restricted HSPC differentiation, which suggested that Vitisin A participated in monocyte generation and carried out the immunomodulation. Together, Vitisin A ameliorates inflammation during atherosclerosis and UC via the suppressed differentiation of HSPCs toward monocytes, which could be considered an ideal functional component with immunomodulatory effects.
Keywords: Vitisin A; atherosclerosis; hematopoietic stem cell; inflammation; ulcerative colitis.