Background: Baicalin is a flavonoid purified from the medicinal plant Scutellaria baicalensis Georgi. It has been reported that baicalin exhibits antibacterial, anti-inflammatory and analgesic effects and can inhibit nuclear factor-ĸB activation. Periodontal disease is a chronic infective disease of the periodontium caused by bacteria present in dental plaque inducing alveolar bone resorption until teeth are lost. Human periodontal ligament (HPDL) is the connective tissue between alveolar bone and tooth. Receptor activator of nuclear factor-ĸB ligand (RANKL), a member of the tumor necrosis factor (TNF) ligand family, plays an important role in osteoclastogenesis from osteoclast precursors to mature osteoclasts. In this study we investigate the effects of baicalin on RANKL protein production and messenger RNA (mRNA) expression induced by IL-1β in cultured HPDL cells. Methods: To induce RANKL expression, IL-1β was added to serum-free medium HPDL cells and incubated. Various concentrations of baicalin (0, 0.001, 0.01 and 0.1 µg/ml) were added to the medium and the cells were treated for 0, 12, 24, 48 and 72 h, respectively. RANKL in the cells was detected using immunocytochemistry. The mRNA of RANKL, osteoprotegerin (OPG) and cyclooxygenase-2 (COX-2) were measured by semiquantitative reverse transcription-polymerase chain reaction. Results: The expression of RANKL at mRNA and protein levels in HPDL cells was stimulated by IL-1β. Baicalin suppressed IL-1β-induced RANKL and COX-2 production at a concentration of 0.01 µg/ml. The most prominent effect was observed with 48 h of baicalin treatment. The inhibition of baicalin on the rhIL-1β-stimulated OPG expression was first apparent at 24 h after the start of treatment, however it did not reach significant differences. Conclusions: The data suggest that baicalin may inhibit RANKL mRNA expression via the suppression of COX-2 expression induced by IL-1β. In addition to its antibacterial and anti-inflammatory properties, baicalin was shown to be effective in periodontitis and alveolar bone resorption.

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