Use LPS

LPS signal via MyD88 and also by TRIF adapter proteins. While MyD88 pathway induce proinflammatory cytokines, TRIF pathway induce Typ1 I interferons (IFN beta) which induce IL-10

Also, IL-10 can be induced as an anti-inflammatory loop following a pro-inflammatory stimuli. Depending of how long you leave LPS into the cells, TNFa or IL-1 cytokines would signal back and induce IL-10. Although is also right that LPS would directly induce IL-10, most likely as a contra balance mechanism to limit inflammation. 

Thank you all for your great answers.I really appreciate it. As everyone suggested LPS indeed a good candidate to induce IL10. But initially LPS treatment results in MAPK/NF-κB activation which results in inflammation/pro-inflammatory cytokine production. I want to induce anti-inflammatory pathways in vivo. The main goal is to produce maximum IL10 and polarize activated macrophages to M2c macrophages to resolve inflammation quickly. 

If you look at TLR4 antagonists such as curcumin , Punicalagin , Chitohexaose , Baicalin etc they all inhibit TLR4-MAPK/NF-κB pathway thus polarizing activated macrophages to M2c which express high level of IL10.

So what is the real advantage of using LPS over TLR4 antagonists?