Protective effects of dehydrocostus lactone against hydrogen peroxide-induced dysfunction and oxidative stress in osteoblastic MC3T3-E1 cells.

Oxidative stress regulates cellular functions in multiple pathological conditions, including bone formation by osteoblasic cells. To elucidate the protective effects of dehydrocostus lactone on the response of osteoblast to oxidative stress, osteoblastic MC3T3-E1 cells were incubated with 0.3mM hydrogen peroxide (H(2)O(2)) and/or dehydrocostus lactone (0.1-10 microg/ml), and markers of osteoblast function and oxidative damage were examined. Dehydrocostus lactone (0.1-10 microg/ml) significantly increased osteoblast growth compared with control (P<0.05). H(2)O(2)-induced reduction of differentiation markers such as alkaline phosphatase (ALP), collagen content, and calcium deposition was recovered in the presence of dehydrocostus lactone (0.4-2 microg/ml). Treatment with dehydrocostus lactone (10 microg/ml) decreased the production of osteoclast differentiation-inducing factors such as interleukin (IL)-6 and receptor activator of nuclear factor-kB ligand (RANKL) in the presence of H(2)O(2). Moreover, dehydrocostus lactone (0.4-2 microg/ml) decreased the formation of protein carbonyl (PCO) and malondialdehyde (MDA) induced by H(2)O(2) in osteoblasts. Taken together, these results demonstrate that dehydrocostus lactone can protect osteoblasts against H(2)O(2)-induced cellular dysfunction. These results also suggest that dehydrocostus lactone may be valuable as a protective agent against oxidative damage in osteoblasts.