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Anti-tumor effects of Solanum nigrum L. extraction on C6 high-grade glioma

细胞凋亡 流式细胞术 膜联蛋白 细胞生长 癌症研究 胶质瘤 免疫印迹 细胞周期 活力测定 生物 分子生物学 化学 生物化学 基因
作者
Jiahui Li,Song-ya Li,Ming-Xue Shen,Runze Qiu,Hongwei Fan,Yingbin Li
出处
期刊:Journal of Ethnopharmacology [Elsevier BV]
卷期号:274: 114034-114034 被引量:30
标识
DOI:10.1016/j.jep.2021.114034
摘要

Abstract Ethnopharmacological relevance Solanum nigrum L. (SN) is a traditional Chinese medicine with anti-tumor effects, has been used in cancer for centuries, but the role on high-grade gliomas (HGG) is not clear. Aim of the study This work was to investigate the anti-tumor effects of SN extract on rat C6 glioma in vitro and in vivo, providing a new medium for the treatment of HGG. Materials and methods After identification and quality inspection of SN medicinal materials by HPLC-MS/MS and HPLC, CCK8 and colony formation assay were conducted to study the effects of SN on vitality and proliferation of C6 cells. Cell morphology was evaluated by HE staining, and flow cytometry was used for apoptosis analysis. The effects on cell migration and invasion were determined by transwell and wound healing assay. Western blot was used to further investigate the influence of SN on migration, invasion and apoptosis of tumor cells. In addition, the rat intracranial transplanted tumor model was used to evaluate the effects of SN on growth and infiltration of tumor and proliferation of transplanted tumor cells. Results SN extract suppressed the viability of C6 cells in a dose-dependent manner. The extract attenuated cell cloning, migration and invasion, and induced cell Annexin V+ PI+ late-stage apoptosis. Besides, SN induced the expression of apoptotic proteins including Bax and Cleaved Caspase-3, downregulated anti-apoptotic protein Bcl-2, and decreased the level of migratory proteins MMP-2 and MMP-9. Moreover, SN reduced the growth and infiltration of C6 glioma tissue and suppressed the proliferation of tumor cells in rat brain. Conclusions SN extract has significant inhibitory activity on the growth and invasion of C6 HGG in vivo and in vitro.

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