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Arctigenin promotes bone formation involving PI3K/Akt/PPARγ signaling pathway.
Chemical Biology & Drug Design ( IF 3.2 ) Pub Date : 2020-01-14 , DOI: 10.1111/cbdd.13659 Hongbo Li 1 , Chunli Yang 2 , Min Lan 1 , Xingen Liao 1 , Zhiming Tang 1
Chemical Biology & Drug Design ( IF 3.2 ) Pub Date : 2020-01-14 , DOI: 10.1111/cbdd.13659 Hongbo Li 1 , Chunli Yang 2 , Min Lan 1 , Xingen Liao 1 , Zhiming Tang 1
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This study investigated the mechanisms through which arctigenin promotes osteogenesis. Bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (OVX) rats were differentiated into osteoblasts, and osteogenesis was evaluated via Alizarin Red S (ARS) staining and alkaline phosphatase (ALP) measurements in cultured BMSCs. The levels of phosphorylated AKT serine/threonine kinase 1 (p-Akt), and peroxisome proliferator-activated receptor gamma (PPARγ) expression were quantified by Western blot analysis. The levels of urine calcium (U-Ca), urine phosphorus (U-P), serum ALP, and bone mineral density (BMD) of OVX rats were assessed in vivo. The results showed that treatment with arctigenin in rat BMSCs enhanced mineralization, increased ALP activity, increased the expression of Akt and p-Akt, and decreased PPARγ expression, consistent with its ability to promote osteoblast differentiation. Furthermore, arctigenin prevented OVX-induced osteoporosis in rats by increasing BMD and ALP activity and inhibiting the loss of Ca and P. In contrast, treatment with LY294002, a selective inhibitor of the phosphatidylinositol 3-kinase (PI3K), produced the opposite phenotype. These data suggest that the protective effects of arctigenin on BMSCs and OVX rat models result from the induction of osteogenesis involving the PI3K/Akt/PPARγ axis.
中文翻译：
Arctigenin促进涉及PI3K / Akt /PPARγ信号传导途径的骨形成。
这项研究调查了Arctigenin促进成骨的机制。将来自卵巢切除（OVX）大鼠的骨髓间充质干细胞（BMSC）分化为成骨细胞，并通过在培养的BMSC中通过茜素红S（ARS）染色和碱性磷酸酶（ALP）测量评估成骨作用。磷酸化的AKT丝氨酸/苏氨酸激酶1（p-Akt）和过氧化物酶体增殖物激活受体γ（PPARγ）表达的水平通过蛋白质印迹分析进行定量。在体内评估了OVX大鼠的尿钙（U-Ca），尿磷（UP），血清ALP和骨矿物质密度（BMD）的水平。结果表明，在大鼠骨髓间充质干细胞中arctigenin处理可增强矿化作用，增加ALP活性，增加Akt和p-Akt的表达，并降低PPARγ的表达，与其促进成骨细胞分化的能力相一致。此外，Arctigenin可通过增加BMD和ALP活性并抑制Ca和P的丢失来预防OVX诱导的大鼠骨质疏松。相反，用磷脂酰肌醇3-激酶（PI3K）的选择性抑制剂LY294002处理产生相反的表型。这些数据表明，Arctigenin对BMSCs和OVX大鼠模型的保护作用是由诱导涉及PI3K / Akt /PPARγ轴的成骨作用引起的。
更新日期：2020-01-14
中文翻译：
Arctigenin促进涉及PI3K / Akt /PPARγ信号传导途径的骨形成。
这项研究调查了Arctigenin促进成骨的机制。将来自卵巢切除（OVX）大鼠的骨髓间充质干细胞（BMSC）分化为成骨细胞，并通过在培养的BMSC中通过茜素红S（ARS）染色和碱性磷酸酶（ALP）测量评估成骨作用。磷酸化的AKT丝氨酸/苏氨酸激酶1（p-Akt）和过氧化物酶体增殖物激活受体γ（PPARγ）表达的水平通过蛋白质印迹分析进行定量。在体内评估了OVX大鼠的尿钙（U-Ca），尿磷（UP），血清ALP和骨矿物质密度（BMD）的水平。结果表明，在大鼠骨髓间充质干细胞中arctigenin处理可增强矿化作用，增加ALP活性，增加Akt和p-Akt的表达，并降低PPARγ的表达，与其促进成骨细胞分化的能力相一致。此外，Arctigenin可通过增加BMD和ALP活性并抑制Ca和P的丢失来预防OVX诱导的大鼠骨质疏松。相反，用磷脂酰肌醇3-激酶（PI3K）的选择性抑制剂LY294002处理产生相反的表型。这些数据表明，Arctigenin对BMSCs和OVX大鼠模型的保护作用是由诱导涉及PI3K / Akt /PPARγ轴的成骨作用引起的。
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