Pharmacology of Ginger
Bioactive constituents of ginger such as 6-shogaol have shown potent in vitro and in vivo anticancer activity against ovarian, Hepatoma liver, colon and other cancers
In vitro research by Rhode et al. (2007) demonstrated that treatment of cultured ovarian cell lines (A2780, SKOV3 and ES2) with ginger extract induced profound growth inhibition; all cell lines were tested at a concentration around 100 µg/mL. Rhode et al. (2007) found that 6-shogaol in ginger extract was the most active constituent and that ginger extract inhibited the NFκB activation as well as diminished secretion of VEGF and IL-8.
The in vitro results of Rhode et al. (2007) were confirmed by Habib et al., 2008 by in vivo studies. These researchers produced data that indicates ginger extracts may act as anti-cancer and anti-inflammatory agents by inactivating NFκB through the suppression of the pro-inflammatory TNF-α. Ginger extracts were able to significantly reduce the elevated expression of NFκB by 63% and TNF- by 91% in rats with liver cancer. Ginger extract was able to reduce the incidence of liver neoplasms in rats by 83%.
Further proof that ginger has anti-cancer properties was demonstrated by Sharma et al. (2009) with findings that ginger may exhibit its anti-neoplastic effects in cervical cancer. They observed that treatment of human cervical carcinoma cell line HeLa, with ethanolic ginger extract in combination with gemcitabine, resulted in significant dose-dependent decrease in cell viability and increased the efficacy of gemcitabine while being minimally toxic to normal cells. They concluded that ginger can be used in combination with chemotherapeutic drugs to increase their efficacy and reduce their side effects.
Chen et al. (2007) presented evidence that 6-shogaol, an alkanone isolated from the rhizomes of ginger, can effectively induce apoptotic cell death of human hepatoma p53 mutant Mahlavu cells via an oxidative stress-mediated caspase-dependent mechanism. Mahlavu cells, poorly differentiated and p53 mutants of a human hepatoma subline, are known to be highly refractory to a number of chemotherapy agents and radiotherapy due to their high expressions of multidrug resistance gene-1 (MDR-1) and Bcl-3 proteins. The cascade of events in 6-shogaol apoptosis of Mahlavu cells involved an initial overproduction or reactive oxygen species (ROS) followed by a severe depletion of intracellular glutathione (GSH) contents. Further, the data suggests that the near complete suppression of 6-shogaol induced apoptosis by N-acetylcysteine (NAC) and GSH confirms the idea that the GSH depletion is the major contributing factor involved in the arbitration of apoptosis.
Ali et al. (2008) report that the phenolic alkanone 6-gingerol and the related compound 6-shogaol reduced gastric cancer cells via different mechanisms (Ishiguro et al., 2007). The former compound affected the viability of cancer cells only slightly, while the latter has a significant inhibitory effect by damaging microtubules and inducing mitotic arrest.