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-kappa B (NF-kappa B) 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-la (MIP-1 alpha). RT-qPCR demonstrated that naringin significantly reduced the LPS-induced upregulation of IL-8, MCP-1 and MIP-1 alpha mRNA expression in a dose-dependent manner. Additionally, western blot analysis revealed that naringin effectively suppressed NF-kappa B activation by inhibiting the degradation of I kappa B-alpha 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-I and MIP-1 alpha secretion and mRNA expression, possibly by blocking the activation of the NF-kappa B and MAPK signaling pathways in LPS-induced RAW 264.7 macrophages.