Chlorogenic acid suppresses lipopolysaccharide-induced nitric oxide and interleukin-1β expression by inhibiting JAK2/STAT3 activation in RAW264.7 cells

Chlorogenic acid (CA) is a phenolic compound purified from coffee, fruits and their associated beverages, which possess various biological properties, such as antioxidant and anticarcinogenic activities. The present study evaluated the effects of CA on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 cells and the associated intracellular signaling pathways using reverse transcription-quantitative polymerase chain reaction, western blotting and enzyme-linked immunosorbent assays. CA pretreatment inhibited LPS-induced expression of inducible nitric oxide synthase (iNOS), nitric oxide (NO) and pro-inflammatory mediators including interleukin (IL)-6, tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein-2 (MIP-2) and IL-1 beta in RAW264.7 cells. In addition, phosphorylation of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) with LPS was inhibited by CA pretreatment. CA and STAT3 inhibitor (STAT3i) pretreatment inhibited LPS-induced nuclear translocation of phosphorylated STAT3. In addition, STAT3i inhibited the LPS-induced expression of iNOS, NO and IL-1 beta similar to the results of CA pretreatment. By contrast, STAT3i did not inhibit the LPS-induced increase in IL-6, TNF-alpha and MIP-2 expression. These results indicate that CA may suppress LPS-induced NO and IL-1 beta expression by inhibiting JAK2/STAT3 activation in RAW264.7 cells.