Tetrandrine Inhibits Cell Proliferation and Induces Apoptosis of Human Hepatocarcinoma through Influencing the Function of Cell Membrane

被引:0
|
作者
Ji, Yubin [1 ,2 ]
Wei, Chi [1 ]
He, Jiaxin [2 ]
Xin, Guosong [1 ,2 ]
Yu, Miao [1 ]
机构
[1] Harbin Univ Commerce, Ctr Res & Dev Life Sci & Environm Sci, Harbin 150076, Peoples R China
[2] Minist Educ, Engn Res Ctr Nat Anticanc Drugs, Harbin 150076, Peoples R China
来源
LATIN AMERICAN JOURNAL OF PHARMACY | 2020年 / 39卷 / 02期
基金
中国博士后科学基金;
关键词
Tetrandrine; Apoptosis; Tumor cell membrane; Membrane protein; Ion channel;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The purpose of the study covered in this paper was to probe into the inhibitory effect of tetrandrine on HepG-2 hepatocellular carcinoma cells by destroying tumor cell membrane function. The CCK-8 results indicated that tetrandrine caused significant reduction on the proliferation of HepG-2 cells. While observed with fluorescent microscopy and inverted microscopy, morphological alterations caused by apoptosis were identified subsequent to tetrandrine administration. Compared with control group, the tetrandrine treatment group had significantly elevated apoptosis rate, according to flow cytometry. In addition, changes of membrane functional components (protein, cholesterol, and sialic acid) were detected. Cell membrane fluidity was measured by fluorescence polarization. Blocking degree of HepG-2 cells membrane was measured by chromameter. Results showed that tetrandrine could reduce the functional components of tumor cell membranes and decrease the fluidity and blocking degree of HepG-2 cell membrane. Meanwhile, tetrandrine could decrease the activities of Na+/K+-ATPase and Ca2+/Mg2+-ATPase was also observed by ATPase activity assay. Tetrandrine significantly down-regulated GLUT-1 and LAT-1 levels and compared with control group, according to western blot assay findings. In conclusion, tetrandrine can reduce the fluidity and blocking degree of cell membrane by reducing the content of total protein, cholesterol and sialic acid content of HepG-2 cells. Moreover, it can destroy the homeostasis of tumor cell internal environment, reduce the supply of cell nutrients by reducing the activity of ion transporters, down-regulating the expression of glucose and amino acid transporter, and ultimately all the above facilitate the trigger of apoptosis of malignant HepG-2 cells.
引用
收藏
页码:331 / 340
页数:10
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