Low concentration of lipopolysaccharide acts on MC3T3-E1 osteoblasts and induces proliferation via the COX-2-independent NFkB 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 (PGE2) production, which induces the nuclear factor kappa B (NFB) activation and is beneficial to fracture healing. In order to know their roles in skeletal regeneration, mouse MC3T3-E1 osteoblasts were treated with NFB inhibitor BAY 11-7082 and sc791 (a selective COX-2 inhibitor), in the presence of LPS. Interestingly, LPS could induce osteoblasts proliferation through increasing NFB activation and translocation. This induction was not related to COX-2 expression, suggesting that LPS-induced NFB activiation is independent of COX-2. It is possible that low concentration of LPS can act as a stimulating factor of the NFB pathway in nonstimulated cells such as osteoblasts. COX-2 is not necessary for the NFB 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.