Sun Xi, Gan Lijun, Li Nan, Sun Shuyi, Li Na
Department of Neonatology, First Hospital of Jilin University, No. 71 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, China.
Department of Ultrasonography, Jilin Provincial People's Hospital, Changchun, 130000, Jilin, China.
AMB Express. 2020 Sep 11;10(1):165. doi: 10.1186/s13568-020-01098-0.
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.
我们探究了长春花碱（Tab）如何预防地塞米松（Dex）诱导的骨质疏松症。将成骨细胞用Dex（100 μM）处理，同时分别添加或不添加Tab（5或10 μM）。我们测量了细胞活力、碱性磷酸酶（ALP）活性、线粒体超氧化物和活性氧水平。我们使用流式细胞术探究Tab对线粒体膜电位和成骨细胞凋亡的影响。我们使用逆转录聚合酶链反应（RT-PCR）和蛋白质印迹法检测Tab对蛋白质表达的影响。我们评估了Tab对Dex诱导的骨质疏松症大鼠骨组织病理学和骨密度的影响。Tab增加了细胞活力和ALP活性，并降低了线粒体超氧化物、活性氧和基质金属蛋白酶水平以及成骨细胞凋亡。Tab显著降低了核因子红细胞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，它增加了编码矮小相关转录因子2、骨形态发生蛋白-2和osterix的mRNA水平。这些数据表明，Tab通过调节Nrf2信号通路改善Dex诱导的骨质疏松症。
