巴戟天多糖通过调节 miR-214-3p/NEDD4L 抑制绝经后骨质疏松症小鼠的破骨细胞分化

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-11-01 Epub Date: 2024-08-28 DOI:10.1007/s00223-024-01271-8
Hui Huang, Jian Chen, Xiaomei Lin, Zhengkun Lin
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引用次数: 0

摘要

研究巴戟天多糖(MOPs)通过miR-214-3p及其靶蛋白调节破骨细胞分化和凋亡的潜在机制。对8周龄的雌性C57BL6小鼠进行卵巢切除术,建立绝经后骨质疏松症(PMOP)模型。小鼠立即接受每公斤 500 毫克的澳门巴黎人娱乐官网治疗(预防组);其他小鼠在手术后 2 周接受澳门巴黎人娱乐官网治疗(治疗组)。检测左股骨骨矿密度(BMD)。给 RAW264.7 细胞注射 NF-κB 配体受体激活剂(RANKL)以建立破骨细胞(OC)模型,并用含 1 或 2 g/kg MOPs 的血清进行处理。通过 Western 印迹、定量实时逆转录聚合酶链反应(qRT-PCR)和流式细胞术检测凋亡相关指标、miR-214-3p 和表达发育下调 4-Like(NEDD4L)。OC接受miR-214-3p抑制剂或NEDD4L小干扰RNA(siRNA)。澳门巴黎人娱乐官网逆转了PMOP诱导的骨骼变化。与 RANKL 组相比,MOPs 增加了 OCs 的凋亡和相关标记物。MOPs降低了PMOP小鼠股骨的miR-214-3p(P
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Morinda Officinalis Polysaccharides Inhibit Osteoclast Differentiation by Regulating miR-214-3p/NEDD4L in Postmenopausal Osteoporosis Mice.

Morinda Officinalis Polysaccharides Inhibit Osteoclast Differentiation by Regulating miR-214-3p/NEDD4L in Postmenopausal Osteoporosis Mice.

To investigate the potential mechanism of Morinda officinalis F. C. How polysaccharides (MOPs) in regulating osteoclast differentiation and apoptosis through miR-214-3p and its target protein. Ovariectomy was performed in 8-week female C57BL6 mice to establish the postmenopausal osteoporosis (PMOP) model. Mice were treated immediately with 500 mg/kg of MOPs (prevention group); others were treated 2 weeks after operation (treatment group). Left femur bone mineral density (BMD) was examined. RAW264.7 cells were administered with receptor activator of NF-κB ligand (RANKL) to establish the osteoclast (OC) model and treated with serum containing 1 or 2 g/kg of MOPs. Apoptosis-related indexes, miR-214-3p, and Expressed Developmentally Down-regulated 4-Like (NEDD4L) were detected by western blot, quantitative real-time-reverse transcription polymerase chain reaction (qRT-PCR), and flow cytometry. OC received a miR-214-3p inhibitor or NEDD4L small interfering RNA (siRNA). MOPs reversed the PMOP-induced changes in bones. Compared with the RANKL group, MOPs increased the apoptosis and related markers in OCs. MOPs decreased the femur miR-214-3p of PMOP mice (P < 0.001). Higher concentrations of MOPs reversed the upregulation of miR-214 mRNA in OCs (P < 0.001). miR-214-3p inhibitor increased the expression of Bax and CC3 (P < 0.01) and decreased the expression of Bcl-2 (P < 0.05). NEDD4L is targeted by miR-214. NEDD4L was upregulated in the RANKL + MOPs group (P < 0.01). miR-214-3p inhibitor increased the upregulation of NEDD4L induced by MOPs (P < 0.05). siRNA NEDD4L significantly reversed the inhibition of MOPs on osteoclast differentiation with miR-214-3p inhibitor (P < 0.01). MOPs effectively prevent PMOP by inhibiting osteoclastogenesis and inducing OC apoptosis through the miR-214-3p/NEDD4L pathway.

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CiteScore
7.20
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4.30%
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