RESUMEN
Diets rich in n-3 polyunsaturated fatty acid (n-3 PUFA) fish oil (FO) have beneficial effects in obesityassociated metabolic disease. However, contradictory roles in inflammatory disease intervention have been reported. Our previous work revealed that a highFO diet promoted myeloid cell differentiation by modifying the bone marrow microenvironment; however, its effects on liver inflammation and complement system activation remain unknown. By performing ELISA, reverse transcriptionquantitative polymerase chain reaction, flow cytometry and histology on mice fed with highFO and lowfat diets, the present study demonstrated that a 4week highFO diet promoted liver inflammation in mice without affecting body or liver weight. The livers of highFO diet mice exhibited increased infiltration of T cells and CD11b+ Gr1+ myeloid cells. Additionally, a higher level of IL1ß and MCP1 mRNA expression was detected, suggesting that the highFO diet promoted liver inflammation. Further experiments indicated that the highFO diet increased the total hemolytic complement activity (CH50), promoted the production of the membrane attack complex and increased the levels of various complement proteins in vivo, including complement components C3, C4b, C1qb and factor B. Furthermore, higher concentrations of triglyceride were detected in the peripheral blood of highFO diet mice, indicating the potential protective roles of n3 PUFAs in FO against lipotoxicity in hyperlipidemia. Collectively, the present study demonstrated that high FO intake induced inflammation and activated the complement system in the liver. However, further study is required to determine the exact mechanisms.