Figure 7. Proposed mechanism of the anti-inflammatory effects by BPIS induced.

LPS directly promoted the TLR4 activation, triggering its inflammatory pathways. BPIS treatment promoted the ROS accumulation, and led to the increase of miR-149 expression. Further, miR-149 directly targeted the 3′-UTR of Akt to block NF-kB nuclear translocation, and then attenuated expression of pro-inflammatory factors (IL-1β, IL-8 and IL-6) in LPS-induced HT-29 cells.