calcusyn software to calculate ci values

In addition, the activity of apoptosis induction and metastasis suppression by CK was also described in several cancer cell lines ( 8- 11).

It has been reported that CK could inhibit the proliferation of myeloid leukemia, pulmonary adenocarcinoma, gastric adenocarcinoma and hepatoma cell lines ( 5- 7). After orally taken, ginsenosides are metabolized in intestine by bacteria to produce several active metabolites that have been shown to possess anti-tumor effects in various types of cancer through modulations of different signaling pathways ( 2- 4).Īs a major metabolite of protopanaxadiol type ginsenosides, compound K (CK) is one of the best-studied for its anti-cancer activities. The difference between these two families is the presence of the hydroxy group at C-6 position ( 1). Ginsenosides are categorized into two main classes based on the structure, e.g., the protopanaxadiol- and protopanaxatriol-families. Dammarane-type tetracyclic triterpenoid saponins, also known as ginsenosides, are well accepted as the major ingredients responsible for the pharmaceutical functions of ginseng ( 1). Panax Ginseng has been widely used as a preventive and/or therapeutic herbal medicine, especially in oriental countries, for a long time. Keywords: Compound K (CK) cisplatin ginsenoside lung cancer In the present study, our data provide the first evidence that CK could be potentially used as an agent to synergize the efficacy of cisplatin in lung cancer. Novel discoveries of low toxicity compounds to improve the outcome or enhance the efficacy of chemotherapies are of great interest. Furthermore, by using p53-null lung cancer cells, we demonstrate that the synergy was p53 dependent.Ĭonclusions: Conventional chemotherapies are often accompanied by development of drug resistance and severe side effects. In addition, the ability of cisplatin in apoptosis induction was similarly synergized by CK. Consequently, synergistic inhibition of cell growth was observed when the cells were co-treated with CK and cisplatin compared to single treatment.

Results: We found that CK could significantly enhance cisplatin-induced p53 expression and activity in two lung cancer cell lines, H460 and A549.

Combination index (CI) was calculated to determine synergism. MTT assay and TUNEL staining were employed to investigate the drug effects on cell growth and apoptosis, respectively. Methods: Western blotting and p53 reporter assay were used to assess p53 expression and activity. Objective: To evaluate the potential of ginsenoside metabolite compound K (CK) in enhancing the anti-tumor effects of cisplatin against lung cancer cells, including cell proliferation and apoptosis, and the underlying mechanism.

Calcusyn software to calculate ci values