Effect of celastrol on anti-proliferation and energy metabolism in SGC-7901 cells and ECV304 cells
10.7501/j.issn.0253-2670.2016.21.017
- Author:
Shu-Jing WANG
1
Author Information
1. College of Pharmacy Harbin University of Commerce
- Publication Type:Journal Article
- Keywords:
Antitumor;
Celastrol;
Energy metabolism;
Glycolysis;
Hexokinase;
Hypoxia inducible factor;
Lactate dehydrogenase;
Monocarboxylate transporter;
Pyruvate kinase
- From:
Chinese Traditional and Herbal Drugs
2016;47(21):3854-3860
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the activity of celastrol on the proliferation and the mechanism of energy metabolism to human gastric cancer cells (SGC-7901) and human umbilical vein endothelial cells (ECV304). Methods: SGC-7901 and ECV304 were determined to analyze the proliferation inhibitory rate of celastrol to two kinds of cells by MTT method and growth curve; HE staining method was used to observe the morphological changes; Using spectrophotometric method, the activities of the enzymes in glycolytic pathway (hexokinase, pyruvate kinase, and lactate dehydrogenase) were determined, the enzyme in the tricarboxylic acid cycle (succinate dehydrogenase), and the level of ATP which was the end-products in energy metabolism were determined; The Western blotting method was used to determine the expression levels of hypoxia inducible factor (HIF-1α) and single carboxyl transporter (MCF-4). Results: The proliferation inhibition of celastrol to SGC-7901 and ECV304 cells showed in a time-and dose-dependent manner, led to morphologic changes of cells, reduced the activity of HK, LDH, and SDH, lowered the level of ATP; There was no effect to PK. The protein expression levels of HIF-1α and MCF-4 were significantly reduced. The inhibition of celastrol to SGC-7901 was stronger than that of ECV304 cells. Conclusion: Celastrol influence energy metabolism of the two cells by reducing the expression levels of HIF-1α and MCF-4 is significant, and then proliferation can be inhibited. It shows a double inhibition on human gastric cancer cells and angiogenesis of tumor.
