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Flavonoid compound breviscapine suppresses human osteosarcoma Saos-2 progression property and induces apoptosis by regulating mitochondria-dependent pathway.
Journal of Biochemical and Molecular Toxicology ( IF 3.6 ) Pub Date : 2020-09-24 , DOI: 10.1002/jbt.22633
Zhijun Wang 1 , Hongyan Li 2 , Jiyuan Yan 3 , Yang Liu 1
Affiliation  

This study was aimed to investigate the ability of a flavonoid compound breviscapine (BVP) to suppress growth and elicit apoptosis in human osteosarcoma (OS) Saos‐2 cells. The cells were cultured in vitro and treated with three concentrations of BVP (80, 160, and 320 μg/ml). Moreover, C57 mice were injected with Saos‐2 cells to establish a subcutaneous xenograft model, and they were subsequently treated with three doses of BVP via intraperitoneal injection. The viability of the cells was examined by the Cell Counting Kit‐8 method. The apoptotic cells were assessed by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The tumor volume and weight were monitored from day 3 through day 21 after the last injection. The expression of bax, bcl‐2, and cytochrome c (cyt c) mRNA was detected by a real‐time polymerase chain reaction. The protein levels of bax, bcl‐2, cyt c, caspase 3, and caspase 9 were evaluated by Western blot. The expression and distribution of bcl‐2 and bax in tissues were detected by immunohistochemistry. Compared with the control group, BVP treatment inhibited cell proliferation and induced apoptosis of Saos‐2 cells in vitro. Consistently, treatment of mice bearing transplanted tumors with BVP suppressed the growth of OS tumors and promoted cell apoptosis; it also reduced tumor volume and weight. Mechanistically, BVP‐induced apoptosis was mediated by the mitochondria‐dependent pathway, as evidenced by the increased expression of bax and cyt c and the decreased expression of bcl‐2, as well as activation of caspase 9 and caspase 3 in vitro and in vitro. Collectively, BVP inhibits growth and promotes apoptosis of OS by activating the mitochondrial apoptosis pathway.

中文翻译:

黄酮类化合物灯盏花素通过调节线粒体依赖性途径抑制人骨肉瘤 Saos-2 进展特性并诱导细胞凋亡。

本研究旨在探讨类黄酮化合物灯盏花素 (BVP) 抑制人骨肉瘤 (OS) Saos-2 细胞生长和诱导细胞凋亡的能力。细胞在体外培养并用三种浓度的 BVP(80、160 和 320 μg/ml)处理。此外,C57小鼠注射Saos-2细胞建立皮下异种移植模型,随后通过腹腔注射给予三剂量的BVP治疗。通过细胞计数试剂盒-8方法检查细胞的活力。通过流式细胞术和末端脱氧核苷酸转移酶 dUTP 缺口末端标记染色来评估凋亡细胞。最后一次注射后第3天至第21天监测肿瘤体积和重量。通过实时聚合酶链式反应检测bax、bcl-2和细胞色素c (cyt c) mRNA的表达。通过蛋白质印迹评估bax、bcl-2、cyt c、caspase 3和caspase 9的蛋白水平。免疫组化法检测组织中bcl-2、bax的表达及分布。与对照组相比,BVP处理在体外抑制了Saos-2细胞的增殖并诱导其凋亡。一致的是,用 BVP 治疗携带移植肿瘤的小鼠可抑制 OS 肿瘤的生长并促进细胞凋亡。它还减少了肿瘤的体积和重量。从机制上讲,BVP 诱导的细胞凋亡是通过线粒体依赖性途径介导的,bax 和 cyt c 表达增加、bcl-2 表达减少以及 caspase 9 和 caspase 3 体外和体外激活证明了这一点。 。总的来说,BVP 通过激活线粒体凋亡途径来抑制生长并促进 OS 凋亡。
更新日期:2020-09-24
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