School of Nursing, Nanjing University of Chinese Medicine, Nanjing, China.
Front Endocrinol (Lausanne). 2023 Aug 17;14:1162415. doi: 10.3389/fendo.2023.1162415. eCollection 2023.
Postmenopausal osteoporosis is the main cause of fractures in women. Resistance exercise has a positive effect on bone mineral density in postmenopausal osteoporosis patients, but its mechanism is unclear. The purpose of this study was to explore the mechanism of resistance exercise in improving ovariectomized osteoporotic rats based on the transcriptome sequencing technique. Eighteen female Sprague-Dawley rats were randomly divided into the sham-operated group, the non-exercise group, and the resistance exercise group. The rat model of postmenopausal osteoporosis was established by bilateral ovariectomy. Ten weeks after the operation, the resistance exercise group received 2 weeks of adaptive training, and 12 weeks of resistance exercise began in the 13th week. The rats were trained 5 days per week, in 4 sets of 3 repetitions per day. After the intervention, all rats were sacrificed, and the body weight, bone mineral density, trabecular bone microarchitecture, and bone biomechanics were examined. At the same time, RNA-seq and enrichment analysis of gene ontology and Kyoto Encyclopedia of Genes and Genomes were performed on the left tibias, followed by Elisa and RT-qPCR verification. It had been found that resistance exercise can effectively counteract the weight gain of ovariectomized osteoporotic rats, and has a good effect on bone mineral density and trabecular bone microarchitecture. Enrichment analysis showed that regulation of gene expression and osteoclast differentiation is the most closely related biological process and signaling pathway shared by RE/Ovx and NE/Ovx groups. Our results revealed that resistance exercise can play a role in inhibiting osteoclast activation and preventing the enhancement of osteoclast bone resorption function in ovariectomized osteoporotic rats by inhibiting Fos/Fosb-regulated TRAP activation and relieving Calcr inhibition, which has important application value in preventing bone loss caused by estrogen deficiency.
绝经后骨质疏松症是女性骨折的主要原因。抗阻运动对绝经后骨质疏松症患者的骨密度有积极影响,但作用机制尚不清楚。本研究旨在基于转录组测序技术探讨抗阻运动改善去卵巢骨质疏松大鼠的作用机制。将 18 只雌性 Sprague-Dawley 大鼠随机分为假手术组、非运动组和抗阻运动组。通过双侧卵巢切除术建立绝经后骨质疏松大鼠模型。术后 10 周,抗阻运动组进行 2 周适应性训练,第 13 周开始进行 12 周抗阻运动。大鼠每周训练 5 天,每天 4 组,每组 3 次。干预结束后,处死所有大鼠,检测体重、骨密度、骨小梁微结构和骨生物力学。同时,对左侧胫骨进行 RNA-seq 和基因本体论和京都基因与基因组百科全书富集分析,随后进行 Elisa 和 RT-qPCR 验证。研究发现,抗阻运动可有效对抗去卵巢骨质疏松大鼠的体重增加,对骨密度和骨小梁微结构有较好的改善作用。富集分析表明,基因表达调控和破骨细胞分化是 RE/Ovx 和 NE/Ovx 两组最密切相关的生物学过程和信号通路。我们的研究结果表明,抗阻运动可通过抑制 Fos/Fosb 调节的 TRAP 激活和缓解 Calcr 抑制,在抑制破骨细胞激活和防止去卵巢骨质疏松大鼠破骨细胞骨吸收功能增强方面发挥作用,在预防雌激素缺乏引起的骨丢失方面具有重要的应用价值。