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首页> 外文期刊>Journal of Cellular Physiology >Anti‐osteoporosis activity of Sanguinarine in preosteoblast MC3T3‐E1 cells and an ovariectomized rat model
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Anti‐osteoporosis activity of Sanguinarine in preosteoblast MC3T3‐E1 cells and an ovariectomized rat model

机译：抗骨质疏松症血根碱的活动preosteoblast MC3T3 E1细胞和一个切除卵巢的老鼠模型

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摘要

Sanguinarine, a benzophenanthridine alkaloid, has been previously demonstrated to exert antimicrobial, anti‐inflammatory, and anti‐tumor activities. A previous study has identified Sanguinarine as a potential drug candidate for osteoporosis treatment by computational bioinformatics analysis. This study further evaluated the effects of Sanguinarine on the differentiation of murine preosteoblast MC3T3‐E1 cells and its anti‐osteoporosis activity in an ovarietomized rat model. Sanguinarine treatment (0.25, 0.5, 1, and 2?μm) of MC3T3‐E1 cells significantly increased alkaline phosphatase (ALP) activity and the phoshporalyation of AMP‐activated protein kinase α subunit (AMPKα), but did not affect cell proliferation. The induction effects of Sanguinarine treatment (2?μm) on ALP activity, AMPKα phosphorylation, Smad1 phosphorylation, and the expression of three osteoblast differentiation‐regulators (bone morphogenetic protein 2 [BMP2], osterix [OSX], and osteoprotegerin [OPG]) were partially reversed by Compound C treatment. More importantly, Sanguinarine treatment promoted bone tissue growth in an ovariectomized (OVX) osteoporosis rat model as evaluated by histological examination, micro‐CT analysis, and serum parameter detection. In conclusion, these results indicate that Sanguinarine induces the differentiation of MC3T3‐E1 cells through the activation of the AMPK/Smad1 signaling pathway. Sanguinarine can stimulate bone growth in vivo and may be an effective drug for osteoporosis treatment.
机译：血根碱、benzophenanthridine生物碱之前施加抗菌,抗高炎症和抗肿瘤活动。血根碱作为潜在药物候选骨质疏松症治疗的计算生物信息学分析。血根碱的影响的评估分化的小鼠preosteoblast MC3T3 E1在一个细胞及其抗骨质疏松应承担的活动ovarietomized鼠模型。(0.25, 0.5, 1和2 ?μm)的MC3T3 E1细胞显著提高碱性磷酸酶(高山)活动的phoshporalyationAMP激活的蛋白激酶应承担的α亚基(AMPKα),但不影响细胞增殖。血根碱治疗诱导的影响(2 ?μm)高山活动,AMPKα磷酸化,Smad1磷酸化和的表达三个成骨细胞分化还是监管机构(骨头形态蛋白2 (BMP2), osterix (OSX),和osteoprotegerin[功能])部分通过复合C治疗逆转。重要的是,血根碱治疗促进了骨在一次切除卵巢的组织生长(OVX)骨质疏松症大鼠模型评估组织学检查、微检测CT分析,血清参数检测。结果表明:血根碱诱发的地理MC3T3 E1细胞的分化的激活AMPK / Smad1信号通路。血根碱能刺激骨骼生长的体内可能是骨质疏松症的有效药物治疗。

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