钛(Ti)基植入物长时间使用后导致松动，引发的磨粒引起的骨溶解是一种严重的并发症。控制过度成骨细胞分化和炎症是防止磨粒引起的骨溶解的关键。本研究评估了从松叶菊(Inula japonica)中分离的一种伪原生物萜二萜，布里坦对体外成骨细胞的成骨细胞分化和体内钛粒子引起的骨溶解的影响。使用TRAP染色、RT-PCR、蛋白质印迹和免疫细胞化学检验，检验了布里坦在小鼠骨髓源性巨噬细胞(BMMs)的成骨细胞分化上的作用。使用微CT和组织形态测量法，在小鼠颅骨溶解模型中评估了布里坦的保护作用。在BMMs中，布里坦在巨噬细胞集落刺激因子和核能因子κ激活受体激动剂的存在下，抑制了成骨细胞分化和F-actin环的形成。布里坦显著降低了BMMs中成骨细胞特异性标志基因的表达，包括酒石酸抗酸磷酸酶、卡捷普辛K、树突状细胞特异性跨膜蛋白、基质金属蛋白酶9和活化T细胞核质1。此外，布里坦减少了B-淋巴细胞诱导的差异化蛋白-1的表达，该蛋白是负调节成骨细胞生成的转录抑制剂，包括干扰素调节因子-8和B细胞淋巴瘤6。相反，布里坦增加了BMMs中抗氧化应激基因的表达水平，即红细胞核2相关因子2、NAD(P)H喹啉quinone氧化还原酶1和血红素氧合酶1。此外，布里坦的给药明显减少了钛粒子引起的颅骨溶解小鼠模型中的骨溶解。根据这些发现，布里坦可能是一种治疗磨粒引起的骨溶解和与成骨细胞相关疾病的潜在治疗药物。

Wear particle‑induced osteolysis is a serious complication that occurs in individuals with titanium (Ti)‑based implants following long‑term usage due to loosening of the implants. The control of excessive osteoclast differentiation and inflammation is essential for protecting against wear particle‑induced osteolysis. The present study evaluated the effect of britanin, a pseudoguaianolide sesquiterpene isolated from Inula japonica, on osteoclastogenesis in vitro and Ti particle‑induced osteolysis in vivo. The effect of britanin was examined in the osteoclastogenesis of mouse bone marrow‑derived macrophages (BMMs) using TRAP staining, RT‑PCR, western blotting and immunocytochemistry. The protective effect of britanin was examined in a mouse calvarial osteolysis model and evaluated using micro‑CT and histomorphometry. Britanin inhibited osteoclast differentiation and F‑actin ring formation in the presence of macrophage colony‑stimulating factor and receptor activator of nuclear factor kB ligand in BMMs. The expression of osteoclast‑specific marker genes, including tartrate‑resistant acid phosphatase, cathepsin K, dendritic cell‑specific transmembrane protein, matrix metallopeptidase 9 and nuclear factor of activated T‑cells cytoplasmic 1, in the BMMs was significantly reduced by britanin. In addition, britanin reduced the expression of B lymphocyte‑induced maturation protein‑1, which is a transcriptional repressor of negative osteoclastogenesis regulators, including interferon regulatory factor‑8 and B‑cell lymphoma 6. Conversely, britanin increased the expression levels of anti‑oxidative stress genes, namely nuclear factor erythroid‑2‑related factor 2, NAD(P)H quinone oxidoreductase 1 and heme oxygenase 1 in the BMMs. Furthermore, the administration of britanin significantly reduced osteolysis in a Ti particle‑induced calvarial osteolysis mouse model. Based on these findings, it is suggested that britanin may be a potential therapeutic agent for wear particle‑induced osteolysis and osteoclast‑associated disease.