We explored how tabersonine (Tab) protected against dexamethasone (Dex)-induced osteoporosis. Osteoblasts were treated with Dex (100 µM) with or without Table (5 or 10 µM). We measured cell viability, alkaline phosphatase (ALP) activity, and mitochondrial superoxide and reactive oxygen species levels. We used flow cytometry to explore the effects of Tab on mitochondrial membrane potential and osteoblast apoptosis. We used RT-PCR and western blotting to examine the effect of Tab on protein expression. We evaluated the effects of Tab on bone histopathology and bone mineral density in rats with Dex-induced osteoporosis. Tab increased cell viability and ALP activity, and reduced the mitochondrial superoxide, reactive oxygen species and matrix metalloproteinase levels and osteoblast apoptosis. Tab significantly reduced the levels of nuclear factor erythroid 2-related factor 2 (Nrf2), haem oxygenase-1 and NAD(P)H quinone dehydrogenase 1. Moreover, it increased the levels of mRNAs encoding runt-related transcription factor 2, bone morphogenetic protein-2 and osterix. These data suggest that Tab ameliorates Dex-induced osteoporosis by regulating the Nrf2 signalling pathway.

中文翻译：

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烟碱通过调节Nrf2 / ROS / Bax信号通路改善地塞米松诱导的骨质疏松大鼠的成骨细胞凋亡。

我们探讨了烟碱（Tab）如何预防地塞米松（Dex）诱导的骨质疏松症。用有或没有表（5或10 µM）的Dex（100 µM）处理成骨细胞。我们测量了细胞活力，碱性磷酸酶（ALP）活性以及线粒体超氧化物和活性氧的含量。我们使用流式细胞仪研究了Tab对线粒体膜电位和成骨细胞凋亡的影响。我们使用RT-PCR和western印迹来检查Tab对蛋白质表达的影响。我们评估了Tab对Dex诱发的骨质疏松症大鼠的骨组织病理学和骨矿物质密度的影响。Tab增加细胞活力和ALP活性，并降低线粒体超氧化物，活性氧和基质金属蛋白酶水平以及成骨细胞凋亡。Tab显着降低了核因子红系2相关因子2（Nrf2），血红素加氧酶-1和NAD（P）H醌脱氢酶1的水平。此外，它增加了编码矮子相关转录因子2的骨形成的mRNA水平。蛋白质2和osterix。这些数据表明，Tab通过调节Nrf2信号通路改善了Dex诱导的骨质疏松症。