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

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

机构信息

Rehabilitation Department, Zhongshan Hospital, Xiamen University, Xiamen, 361004, Fujian, China.

Xiamen Humanity Rehabilitation Hospital, No. 3775 Xianyue Rd, Xiamen, 361006, China.

出版信息

Calcif Tissue Int. 2024 Nov;115(5):673-685. doi: 10.1007/s00223-024-01271-8. Epub 2024 Aug 28.

Abstract

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.

摘要

为了探究桑枝多糖(MOPs)通过 miR-214-3p 及其靶蛋白调控破骨细胞分化和凋亡的潜在机制。对 8 周龄雌性 C57BL6 小鼠进行卵巢切除术以建立绝经后骨质疏松症(PMOP)模型。术后立即给予 500mg/kg MOPs(预防组);其他组在手术后 2 周给予治疗。检测左股骨骨密度(BMD)。用核因子-κB 受体激活剂配体(RANKL)处理 RAW264.7 细胞建立破骨细胞(OC)模型,并以含 1 或 2g/kg MOPs 的血清处理。通过 Western blot、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 样(NEDD4L)。OC 接受 miR-214-3p 抑制剂或 NEDD4L 小干扰 RNA(siRNA)。MOPs 逆转了 PMOP 引起的骨骼变化。与 RANKL 组相比,MOPs 增加了 OCs 的凋亡及相关标志物。MOPs 降低了 PMOP 小鼠股骨 miR-214-3p(P<0.001)。较高浓度的 MOPs 逆转了 OCs 中 miR-214mRNA 的上调(P<0.001)。miR-214-3p 抑制剂增加了 Bax 和 CC3 的表达(P<0.01),降低了 Bcl-2 的表达(P<0.05)。NEDD4L 是 miR-214 的靶标。在 RANKL+MOPs 组中上调 NEDD4L(P<0.01)。miR-214-3p 抑制剂增加了 MOPs 诱导的 NEDD4L 上调(P<0.05)。siRNA NEDD4L 显著逆转了 miR-214-3p 抑制剂对 MOPs 诱导的破骨细胞分化的抑制作用(P<0.01)。MOPs 通过 miR-214-3p/NEDD4L 通路有效抑制破骨细胞生成,诱导 OC 凋亡,从而有效预防 PMOP。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f2/11531433/7d4b187899af/223_2024_1271_Fig1_HTML.jpg

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