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-Lipoic Acid Inhibits Inflammatory Bone Resorption by Suppressing Prostaglandin E₂ Synthesis¹

Department of Cell and Developmental Biology, DRI, BK21 Program, Seoul National University College of Dentistry, Seoul, Korea

-Lipoic acid (LA) has been intensely investigated as a therapeutic agent for several pathological conditions, including diabetic polyneuropathy. In the present study, we examined the effects of LA on osteoclastic bone loss associated with inflammation. LA significantly inhibited IL-1-induced osteoclast formation in cocultures of mouse osteoblasts and bone marrow cells, but LA had only a marginal effect on osteoclastogenesis from bone marrow macrophages induced by receptor activator of NF-B ligand (RANKL). LA inhibited both the sustained up-regulation of RANKL expression and the production of PGE₂ induced by IL-1 in osteoblasts. In addition, treatment with either prostaglandin E₂ (PGE₂) or RANKL rescued IL-1-induced osteoclast formation inhibited by LA or NS398, a specific cyclooxygenase-2 (COX-2) inhibitor, in cocultures. LA blocked IL-1-induced PGE₂ production even in the presence of arachidonic acid, without affecting the expression of COX-2 and membrane-bound PGE₂ synthase. Dihydrolipoic acid (the reduced form of LA), but not LA, attenuated recombinant COX-2 activity in vitro. LA also inhibited osteoclast formation and bone loss induced by IL-1 and LPS in mice. Our results suggest that the reduced form of LA inhibits COX-2 activity, PGE₂ production, and sustained RANKL expression, thereby inhibiting osteoclast formation and bone loss in inflammatory conditions.

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The JI 2006 176: 1-2. [Full Text]  

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