The autocrine action of salidroside on osteoclast during osteoclastogenesis via hypoxia-inducible factor-1α pathway.

Human & experimental toxicology Pub Date : 2024-01-01 DOI:10.1177/09603271241269028

Yutong Jin, Zhengyang Li, Lin Qi, Lingling Zhang, Dandan Gao, Haizhao Liu, Qingwen Cao, Chenchen Tian, Qun Xia, Yue Wang

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Abstract

Background and objective: The objective of this study was to investigate the potential of salidroside (SAL) (a major active compound in Rhodiola rosea L.) in regulating osteoclast differentiation and function by modulating the HIF-1α pathway and its downstream target genes.

Methods: The expression of HIF-1α and its downstream target genes was examined at both mRNA and protein levels in osteoclasts treated with SAL. Immunofluorescence analysis was performed to assess the nuclear translocation and transcriptional activity of HIF-1α in response to SAL. MTT, flow cytometry, qPCR, TRAP staining and bone resorption assays were used to evaluate the potential effect of salidroside on osteoclasts.

Results: SAL enhanced the expression of HIF-1α and its downstream target genes in osteoclasts. Immunofluorescence analysis confirmed the facilitation of HIF-1α nuclear translocation and transcriptional activity by SAL. In addition, SAL enhanced osteoclast viability, differentiation and bone resorption activity in an autocrine manner through HIF-1α/VEGF, IL-6 and ANGPTL4 pathways.

Conclusion: SAL promotes osteoclast proliferation, differentiation and bone resorption through HIF-1α/VEGF, IL-6 and ANGPTL4 pathways.

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在破骨细胞生成过程中，水杨甙通过缺氧诱导因子-1α途径对破骨细胞产生自分泌作用。

背景和目的：本研究旨在探讨红景天苷（SAL）（红景天中的一种主要活性化合物）通过调节 HIF-1α 通路及其下游靶基因来调节破骨细胞分化和功能的潜力：方法：在用 SAL 处理的破骨细胞中检测 HIF-1α 及其下游靶基因在 mRNA 和蛋白质水平上的表达。免疫荧光分析评估了 HIF-1α 在 SAL 作用下的核转位和转录活性。采用 MTT、流式细胞术、qPCR、TRAP 染色和骨吸收试验来评估丹参皂苷对破骨细胞的潜在影响：结果：水杨苷增强了破骨细胞中 HIF-1α 及其下游靶基因的表达。免疫荧光分析证实，水杨酸促进了 HIF-1α 的核转位和转录活性。此外，SAL还通过HIF-1α/VEGF、IL-6和ANGPTL4途径，以自分泌方式增强破骨细胞的活力、分化和骨吸收活性：结论：SAL可通过HIF-1α/VEGF、IL-6和ANGPTL4途径促进破骨细胞增殖、分化和骨吸收。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Human & experimental toxicology

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