ginsenoside-rd and thiazolyl-blue

Ginseng is a representative herbal medicine in Asia and various pharmacological activities of ginsenoside Rd isolated from ginseng have been reported. However, anti-cancer activity and mechanism of ginsenoside Rd in HT29 colon cancer cell lines were not studied yet. We performed proteomic analysis through two-dimensional gel electrophoresis, MALDI-TOF/TOF-MS and database to identify altered protein induced by ginsenoside Rd treatment in HT29. We can identify fourteen proteins contributed to cell growth inhibition induced by Rd. Proteins involved in the inhibition of mitosis (Stathmin1, Microtubule-associated protein RP/EB family and Stratifin) were significantly up- and down-regulated. And proteins associated with apoptosis (Rho GDP dissociation inhibitor, Tropomyosin1 and Annexin5) were significantly changed. Furthermore, ginsenoside Rd in HT29 was involved in cytoprotection, DNA replication and repair, protein synthesis and degradation, metastasis and mutagenesis. It was supposed that ginsenoside Rd contributed to induce anti-cancer activity by complementary functions of these proteins in colon cancer cells.

Topics: Antineoplastic Agents, Phytogenic; Caspase 3; DNA Fragmentation; DNA Replication; Down-Regulation; Electrophoresis, Gel, Two-Dimensional; Ginsenosides; HT29 Cells; Humans; Hydrolysis; Image Interpretation, Computer-Assisted; Indicators and Reagents; Proteome; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; Tetrazolium Salts; Thiazoles; Trypsin

The destruction of cartilage in patients with osteoarthritis occurs due to an imbalance between matrix synthesis and degradation. Cartilage degradation is induced by the activation of matrix metalloproteinases (MMPs). Therefore, this study was conducted to evaluate the cartilage protective effect of Panax ginseng C.A. Meyer (PG).. S12 cells were treated with various concentrations of extract of PG and gensenosides Rd and Rb(3) for 3h, after which 10 ng/ml interleukin-1beta (IL-1beta) was added to the culture media. The levels of MMP3 in the conditioned media were then evaluated using an enzyme-linked immunosorbent assay (ELISA). In addition, reverse transcriptase-polymerase chain reaction (RT-PCR) was used to evaluate the mRNA expression of Type II Collagen and Pro-collagenase. Furthermore, Western blot analysis was performed to identify the roles that PG played in the ERK and p38 signaling pathways.. The MMP3 secretion levels of S12 cells were significantly lowered in response to treatment with PG and gensenosides Rd and Rb(3) at a concentration of 100 microg/ml when compared to cells that were treated with IL-1beta. In addition, PG induced the mRNA expression of Type II Collagen dose dependently. Furthermore, phosphorylated p38 and ERK were detected in S12 articular cartilage cell line that was treated with IL-1beta. PG decreased the phosphorylation of p38, but PG did not exert any effect on phospho-ERK.. These findings indicate that PG and gensenosides Rd and Rb(3) suppress MMP3 secretion and that gensenosides Rd and Rb(3) are the major elements involved in the suppression of MMP3 by PG. Furthermore, the suppression of MMP3 by PG occurs via the inhibition of phospho-p38 activation. Therefore, PG may exert a protective effect against the cartilage degradation of OA.

Topics: Blotting, Western; Cartilage, Articular; Cell Line; Cell Survival; Chromatography, High Pressure Liquid; Collagen Type II; Coloring Agents; Enzyme Inhibitors; Enzyme-Linked Immunosorbent Assay; Ginsenosides; Indicators and Reagents; Interleukin-1beta; Korea; Magnetic Resonance Spectroscopy; Matrix Metalloproteinase 3; Matrix Metalloproteinase Inhibitors; Medicine, East Asian Traditional; p38 Mitogen-Activated Protein Kinases; Panax; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Tetrazolium Salts; Thiazoles