Department of Microbiology, Guangxi Medical University, Nanning, 530021, Guangxi, China; Research Centre for Regenerative Medicine, Guangxi Medical University, Nanning, 530021, Guangxi, China; Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, 530021, Guangxi, China; School of Biomedical Sciences, University of Western Australia, Perth, WA, 6009, Australia.
Department of Biomedical Materials Science, Third Military Medical University, Chongqing, 400038, China; Department of Anatomy, Third Military Medical University, Chongqing, 400038, China; School of Biomedical Sciences, University of Western Australia, Perth, WA, 6009, Australia.
Arch Biochem Biophys. 2018 Jun 1;647:76-83. doi: 10.1016/j.abb.2018.04.011. Epub 2018 Apr 17.
Pathological fractures caused by osteolytic lesions seriously threaten the health of patients. Osteoclasts play important roles in bone resorption whose hyperfunction are closely related to osteolytic lesions. Studies on osteoclast differentiation and function assist in the prevention of excessive bone loss associated diseases. We screened a variety of natural compounds with anti-inflammatory effect and found that poria cocos polysaccharide (PCP) inhibited RANKL-induced osteoclast formation and bone resorption via TRAcP staining, immunofluorescence, RT-PCR and western blot. PCP down-regulated phosphorylation of STAT3, P38, ERK and JNK, and thus repressed the expression of NFAcT1 and c-Fos during RANKL-induced osteoclastogenesis. Besides, the expression of bone resorption related genes such as TRAcP and CTSK was suppressed by PCP. The results suggest that PCP can be invoked as a candidate for the treatment of osteolytic diseases by inhibiting osteoclastogenesis.
溶骨性病变导致的病理性骨折严重威胁着患者的健康。破骨细胞在骨吸收过程中发挥着重要作用，其功能亢进与溶骨性病变密切相关。对破骨细胞分化和功能的研究有助于预防与过度骨丢失相关的疾病。我们筛选了多种具有抗炎作用的天然化合物，发现茯苓多糖（PCP）通过 TRACP 染色、免疫荧光、RT-PCR 和 Western blot 抑制 RANKL 诱导的破骨细胞形成和骨吸收。PCP 下调了 STAT3、P38、ERK 和 JNK 的磷酸化水平，从而抑制了 RANKL 诱导的破骨细胞分化过程中 NFATc1 和 c-Fos 的表达。此外，PCP 还抑制了 TRACP 和 CTSK 等骨吸收相关基因的表达。这些结果表明，PCP 可以通过抑制破骨细胞生成来作为治疗溶骨性疾病的候选药物。
