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Ginsenoside Rd from Panax notoginseng Is Cytotoxic towards HeLa Cancer Cells and Induces Apoptosis
Author(s) -
Yang ZhiGang,
Sun HongXiang,
Ye YiPing
Publication year - 2006
Publication title -
chemistry and biodiversity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.427
H-Index - 70
eISSN - 1612-1880
pISSN - 1612-1872
DOI - 10.1002/cbdv.200690022
Subject(s) - hela , apoptosis , panax notoginseng , cell cycle , chemistry , ginsenoside , microbiology and biotechnology , agarose gel electrophoresis , cytotoxic t cell , cell , viability assay , cancer cell , biology , cancer , biochemistry , dna , in vitro , medicine , pathology , genetics , alternative medicine , ginseng
The saponin ginsenoside Rd ( 1 ), isolated from Panax notoginseng , is used for the treatment of cardiovascular diseases, inflammation, different body pains, trauma, and internal and external bleeding due to injury. In this study, we report that 1 inhibits the cell growth of human cervical cancer (HeLa) cells in a concentration‐ and time‐dependent manner, with an IC 50 value of 150.5±0.8 μg/ml after 48 h of incubation. The drug‐treated cells displayed features of apoptosis, including typical morphological characteristics and formation of DNA ladders, as evident from agarose‐gel electrophoresis. Flow‐cytometric analysis showed that the cell‐cycle distribution of HeLa cells exposed to 1 is characterized by a decrease of the G 0 /G 1 ‐phase and an increase of the S‐phase cells, respectively, in a dose‐dependent manner. The apoptotic rate of HeLa cells treated for 48 h with 210 μg/ml of 1 was 35.8%. Further, 1 was found to increase the expression of Bax and to decrease the expression of Bcl‐2 proteins, respectively, and to lower the mitochondrial transmembrane potential of HeLa cells. The caspase‐3 inhibitor DEVD‐CHO (at 2 μ M ) increased the viability of HeLa cells treated with 1 . Taken together, our study suggests that ginsenoside Rd ( 1 ) significantly inhibits HeLa cell proliferation, and induces cell apoptosis through down‐regulating Bcl‐2 expression, up‐regulating Bax expression, lowering the mitochondrial transmembrane potential, and activating the caspase‐3 pathway. Thus, 1 could serve as a lead to develop novel chemotherapeutic or chemopreventive agents against human cervical cancer.