Low concentration of lipopolysaccharide acts on MC3T3‐E1 osteoblasts and induces proliferation via the COX‐2‐independent NF κ B pathway

The translocations of lipopolysaccharide (LPS) from the gut and its effects on bone healing are usually of clinical interest during bone fracture. As already widely stuided, Cyclooxygenase‐2 (COX‐2) is a key enzyme for prostaglandin E2 (PGE 2 ) production, which induces the nuclear factor kappa B (NF κ B) activation and is beneficial to fracture healing. In order to know their roles in skeletal regeneration, mouse MC3T3‐E1 osteoblasts were treated with NF κ B inhibitor BAY 11‐7082 and sc791 (a selective COX‐2 inhibitor), in the presence of LPS. Interestingly, LPS could induce osteoblasts proliferation through increasing NF κ B activation and translocation. This induction was not related to COX‐2 expression, suggesting that LPS‐induced NF κ B activiation is independent of COX‐2. It is possible that low concentration of LPS can act as a stimulating factor of the NF κ B pathway in nonstimulated cells such as osteoblasts. COX‐2 is not necessary for the NF κ B pathway during LPS‐induced proliferation of osteoblasts since sc791 had no effects on this induction. These studies provide insight into a potential mechanism by which LPS can affect bone tissue repair in the initial phase of inflammation. Copyright © 2009 John Wiley & Sons, Ltd.