Tetrandrine suppresses β‑glucan‑induced macrophage activation via inhibiting NF‑κB, ERK and STAT3 signaling pathways.

Abstract

Macrophages are important in inflammation through the production of various proinflammatory mediators. β‑glucan is a polymer of glucose, which is produced by numerous different organisms, including fungi, and acts as a trigger for the induction of inflammatory responses. Tetrandrine (TET), a bis‑benzylisoquinoline alkaloid isolated from the Chinese herb Radix Stephania tetrandra, has been demonstrated to modulate inflammatory responses. In the present study, it was investigated whether TET affects the inflammatory reaction induced by β‑glucan in murine and human macrophages. It was demonstrated that β‑glucan induced the activation of nuclear factor (NF)‑κB and markedly increased the levels of tumor necrosis factor‑α (TNF‑α) and interleukin1β (IL‑1β) in macrophages. Treatment with TET resulted in downregulation of phosphorylated NF‑κB p65 and reduction of the production of TNF‑α and IL‑1β. In addition, the phosphorylation of ERK and STAT3 was decreased by TET in activated macrophages. Furthermore, it was demonstrated that the inhibitory effects of TET on β‑glucan‑induced macrophage activation was not due to its cytotoxic action. Conclusively, these results indicate that TET can decrease the inflammatory responses mediated by β‑glucan in macrophages. Thus, TET may serve as an effective tool for the treatment of β‑glucan‑associated inflammatory diseases.