Asperosaponin VI protects against bone destructions in collagen induced arthritis by inhibiting osteoclastogenesis

被引：33

作者：

Liu, Kaifei ^{[1
,3
]}

Liu, Ying ^{[2
]}

Xu, Yanting ^{[1
]}

Nandakumar, Kutty Selva ^{[1
]}

Tan, Huijing ^{[1
]}

He, Chonghua ^{[1
]}

Dang, Wenzhen ^{[1
]}

Lin, Jiahe ^{[1
]}

Zhou, Chun ^{[1
]}

机构：

[1] Southern Med Univ, SMU KI United Med Inflammatory Ctr, Sch Pharmaceut Sci, Guangdong Prov Key Lab New Drug Screening, Guangzhou 510515, Guangdong, Peoples R China

[2] Sun Yat Sen Univ, Sch Pharm, Xinhua Coll, Guangzhou 510520, Guangdong, Peoples R China

[3] Jingzhou Cent Hosp, Dept Pharm, Jingzhou 434020, Hubei, Peoples R China

来源：

PHYTOMEDICINE | 2019年 / 63卷

基金：

中国国家自然科学基金;

关键词：

Asperosaponin VI; Osteoclasts; CIA; Bone erosion; Signaling pathway; ADHESION KINASE; DIFFERENTIATION; RESORPTION; MICE; OSTEOARTHRITIS; MECHANISMS; NFAT;

D O I：

10.1016/j.phymed.2019.153006

中图分类号：

Q94 [植物学];

学科分类号：

071001 ;

摘要：

Background: Bone destructive diseases like rheumatoid arthritis (RA), osteoporosis and bone metastatic tumors are mainly mediated by over-activated osteoclasts. Asperosaponin VI (AVI), isolated from the rhizome of Dipsacus asper, belongs to triterpenoid saponins. It has multiple physiological activities but its effects on RA, especially on osteoclast differentiation and activation are still unclear. Purpose: Explore the protective role of AVI on collagen induced arthritis (CIA) in vivo and RANKL induced osteoclastogenesis in vitro. Methods: The effects of AVI on cell viability and RANKL-induced osteoclastogenesis, actin ring formation, bone resorption activity as well as on osteoclast specific gene and protein expression were tested using bone marrow derived monocytes (BMMs). Paws from CIA mice were used for micro-CT, HE and TRAP staining, real-time PCR and western blot. Sera were used for cytokine analysis by ELISA. The signaling pathways were detected using western blot, real-time PCR and immunofluorescence assay. Results: AVI significantly inhibited RANKL-induced osteoclast formation and bone resorption activity by suppressing the formation of actin ring. It also inhibited the expression of various osteoclatogenesis marker genes and signaling pathways. AVI protected arthritis in vivo by suppressing inflammation and bone loss. Conclusion: AVI exerts its anti-osteoclastogenic activity both in vitro and in vivo by inhibiting RANKL-induced osteoclast differentiation and function. Thus, our studies demonstrate a potential therapeutic role for AVI in preventing or inhibiting RANKL-mediated osteolytic bone diseases.

引用

页数：11

共 38 条

[1] The molecular understanding of osteoclast differentiation [J].