Magnolol attenuates the inflammation and enhances phagocytosis through the activation of MAPK, NF-κB signal pathways in vitro and in vivo.

Graphical abstract Highlights • The main problem addressed in this study is the anti-inflammatory effects of Magnolol-a natural extract and the main bioactive component from Magnolia. • U937 LO-2 cells culture and DSS-treated experimental mice were utilized to analyze inflammatory cytokines, proteins activation in MAPK, NF-κB signal pathways regulation, the phagocytosis immunoregulatory effects in vitro and in vivo with that permits analysis of Magnolol contributors to the inflammatory bowel diseases. • By studying living human cell lines, we identified Magnolol previously unknown contributions of enhancement of phagocytosis, specific pro-inflammatory factors IL-6 and IL-1β significantly depression, p-JNK, p-P38, p-IκBα and p-P65 were down-regulation. • We provide experimental evidence to show that Magnolol as a drug could be used to improve human inflammatory bowel disease and gain new insights into the mechanisms involved phagocytosis immunoregulatory effects, MAPK and NF-κB signal pathways. Abstract Magnolol is a natural extract and the main bioactive component from Chinese medicine-Magnolia. We speculate that it's functional action might be associated with the anti-inflammatory effects of magnolol. Herein, the main purpose was to elucidate the phagocytic immune function and anti-inflammatory activities associated. The toxicity of magnolol on U937 and LO-2 cells was assayed by MTT, flow cytometry and laser scanning confocal microscope was utilized to detect the phagocytosis effect on U937 cells, C57BL/6 mice and the follow-up hematoxylin-eosin staining methods were used to evaluate its bioactivity in vivo. The results showed that magnolol had dose dependent effects on enhancement of phagocytosis ability and significantly inhibited the NO production at the concentration range from10 to 40 μM. Furthermore, Magnolol significantly reduced the gene expression and protein release of IL-1β and TNF-α. However, the p-ERK1/2 in MAPK signaling pathway was not significantly affected by magnolol, whereas p-JNK and p-P38 were down-regulated. Magnolol also inhibited the expression of p-IκBα and p-P65 of NF-κB signaling pathways. The loss of body weight and the shorter length of colon were significantly improved in DSS-treated colitis C57BL/6 mice after the administration of magnolol. The cytokines of pro-inflammatory factors TNF-α, IL-6 and IL-1β attenuated significantly in a concentration dependent manner. The histopathological manifestations of 5–20 mg/kg after the treatment magnolol were markedly improved in the DSS-treated mice. These findings showed that magnolol exerted an anti-inflammatory effect through immunoregulatory phagocytosis, MAPK and NF-κB signaling pathways. Our results provide experimental evidence and theory basis for research on anti-inflammatory effects for magnolol as a potentially anti-inflammatory drug candidate. [ABSTRACT FROM AUTHOR]