Naringin inhibits chemokine production in an LPS-induced RAW 264.7 macrophage cell line.

Naringin has been reported to act as an effective anti-inflammatory compound. In a previous study, we demonstrated that the anti-inflammatory effect of naringin on lipopolysaccharide (LPS)-induced acute lung injury in mice correlated with the inhibition of the nuclear factor-κB (NF-κB) pathway. However, the effects and mechanism of action of naringin on LPS-induced chemokine expression are not yet fully understood. This study aimed to evaluate the effect of naringin on chemokine expression in LPS-induced RAW 264.7 macrophages and to provide insights into the possible underlying mechanisms. We found that the in vitro pre-treatment with naringin led to a significant attenuation in the LPS-induced secretion of interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α). RT-qPCR demonstrated that naringin significantly reduced the LPS-induced upregulation of IL-8, MCP-1 and MIP-1α mRNA expression in a dose-dependent manner. Additionally, western blot analysis revealed that naringin effectively suppressed NF-κB activation by inhibiting the degradation of IκB-α and the translocation of p65. Naringin also attenuated MAPK activation by inhibiting the phosphorylation of ERK1/2, JNK and p38 MAPK. Taken together, these demonstrate that naringin reduces IL-8, MCP-1 and MIP-1α secretion and mRNA expression, possibly by blocking the activation of the NF-κB and MAPK signaling pathways in LPS-induced RAW 264.7 macrophages.