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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Shikonin inhibits the proliferation and induces the apoptosis of human HepG2 cells.
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Shikonin inhibits the proliferation and induces the apoptosis of human HepG2 cells.

机译：紫草素抑制人HepG2细胞的增殖并诱导其凋亡。

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摘要

This study investigated the potential of shikonin as an anticancer agent against liver cancer and an in vitro human hepatoma cancer model system. The HepG2 cell line was the hepatoma cancer model in the present study. The inhibitory effect of shikonin on the growth of HepG2 cells was measured by MTT assay. To explore the underlying mechanism of cell growth inhibition of shikonin, the cell cycle distribution, DNA fragmentation, mitochondrial membrane potential (DeltaPsim) disruption, and expression of Bax and Bcl-2 were measured in HepG2 cells. The activity of shikonin in inducing apoptosis was investigated through the detection of Annexin V signal and CD95 expression by flow cytometry and electron microscopy, respectively. Shikonin inhibited the growth of HepG2 cells in a dose-dependent manner. The IC50 value (inhibiting cell growth by 50%) was 4.30 mg/mL. Shikonin inhibited cell growth in a dose-dependent manner and blocked HepG2 cell cycle progression at the S phase. The changes in mitochondrial morphology, dose-dependently decreased in DeltaPsim, were observed in different concentrations of the drug treatment group. Western blot analysis showed that cajanol inhibited Bcl-2 expression and induced Bax expression. Furthermore, we show that shikonin increases Annexin V signal and CD95 (Fas/APO) expression, resulting in apoptotic cell death of HepG2 cells. In addition, lump formation of intranuclear chromatin, pyknosis of cell nucleus, deletion of microvillus, vacuolar degeneration of mitochondria, reduction of rough endoplasmic reticulum, and resolution of free ribosome, etc., associated with apoptosis were discovered by electron microscopy in HepG2 cells after 48 h treatment. Shikonin inhibited HepG2 cells, possibly through the pathway of inducing early apoptosis, and was beneficial for restoring the apoptotic sensitivity of HepG2 cells by CD95, and should therefore be considered as a candidate agent for the prevention or treatment of human hepatoma.
机译：这项研究调查了紫草素作为抗癌剂对肝癌和体外人肝癌模型系统的潜力。在本研究中，HepG2细胞系是肝癌的癌症模型。用MTT法测定了紫草素对HepG2细胞生长的抑制作用。为了探索紫草素抑制细胞生长的潜在机制，测量了HepG2细胞的细胞周期分布，DNA片段化，线粒体膜电位（DeltaPsim）破坏以及Bax和Bcl-2的表达。通过流式细胞术和电子显微镜分别检测膜联蛋白V信号和CD95表达，研究了紫草素诱导细胞凋亡的活性。紫草素以剂量依赖性方式抑制HepG2细胞的生长。 IC50值（抑制细胞生长50％）为4.30mg / mL。紫草素以剂量依赖性方式抑制细胞生长，并在S期阻断HepG2细胞周期进程。在不同浓度的药物治疗组中观察到线粒体形态的变化，在DeltaPsim中剂量依赖性降低。蛋白质印迹分析表明，cajanol抑制Bcl-2表达并诱导Bax表达。此外，我们表明紫草素增加膜联蛋白V信号和CD95（Fas / APO）的表达，导致HepG2细胞凋亡的细胞死亡。另外，在HepG2细胞接种后，通过电子显微镜观察到了核内染色质的团块形成，细胞核的浓缩，微绒毛的缺失，线粒体的液泡变性，内质网粗糙的减少，游离核糖体的分解等，与凋亡相关。 48小时治疗。 Shikonin可能通过诱导早期凋亡的途径抑制HepG2细胞，并且有利于通过CD95恢复HepG2细胞的凋亡敏感性，因此应被视为预防或治疗人肝癌的候选药物。

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