The objective of the present study was to investigate the molecular mechanisms involved in the activity of [10]-gingerol using A2058 human melanoma cells. [10]-Gingerol inhibited the proliferation of A2058 cells by 50% at a concentration of 52 μM. Such inhibition was dose-dependent accompanied by morphological change indicative of apoptosis. Furthermore, flow cytometric analysis by Annexin V and PI double staining showed that [10]-gingerol increased the extent of apoptosis. Analysis of the mechanism of these events indicated that [10]-gingerol increased the ratio of Bax to Bcl-2, resulting in the activation of caspase-9, caspase-3, and poly-ADP-ribose polymerase in a dose-dependent manner.

Ginger was steamed at 121 o C and 1.5 lb/in 2 for 30 min, dried at 60 o C for 12 h, and each step was repeated nine times. During processing, the lightness (L* value) and yellowness (b* value) decreased from 85.65±0.33 and 26.99±0.20 in the non-treated ginger to 56.91±0.25 and 16.69±0.06 in ginger treated for the ninth treatment. On the other hand, redness (a* value) increased from -1.51±0.03 to 7.34±0.08 on the eight treatment and then decreased to 7.21±0.04 on the ninth theatment. The contents of 6-gingerol decreased from 3.257±0.067 mg/g in the non-treated ginger to 0.567±0.036 mg/g on the theatment, whereas the contents of 6-shogaol increased from 1.299±0.050 mg/g to 2.999±0.089 mg/g on the sixth treatment and decreased to 2.099±0.039 on the ninth treatment. The contents of 10-gingerol decreased slightly from 1.106±0.125 mg/g to 0.806±0.026 mg/g. Unlike the 6- and 10-gingerol, the contents of 8-gingerol did not change greatly, with values between 0.916±0.005 mg/g and 1.106±0.005 mg/g being observed during processing. The tyrosinase inhibitory activities were increased from 43.42±11.45% in the non-treated ginger to 100% on the sixth treatment and then decreased to 51.98±7.36% on the theatment. The antioxidative activity was retained during processing.

6-Gingerol exerts anti-tumor effects in various cancer cell models. We evaluated the effect of 6-gingerol on the growth of MCF-7 breast cancer cells and MCF-10A breast epithelial cells to determine whether any growth-inhibitory effects found were attributable to apoptosis, and to elucidate the underlying mechanism of action. 6-Gingerol inhibited the viability of both cell lines in a dose- and time-dependent manner; however, the degree of inhibition was greater in MCF-7 than MCF-10A cells. By flow cytometry, induction of dose- and time-dependent apoptosis was found, and the magnitude of apoptosis was also markedly greater in MCF-7 than MCF-10A cells. Expression of caspase-3 and poly (ADP-ribose) polymerase (PARP) was observed in MCF-7 cells treated with 6-gingerol, and further cleavage of PARP occurred in these cells. We suggest that 6-gingerol induces apoptosis in human breast cancer cells mainly by promoting caspase-3 expression and subsequent degradation of PARP.

[6]-Gingerol, a major polyphenol of ginger(Zingiber officinale), exhibits a variety ofbiological properties including anti-oxidant, anti-inflammatory and anti-cancer activity. However,the radioprotective effect of [6]-gingerol is still unknown. The aim of this study was to investigatethe radioprotective effect of [6]-gingerol against radiation-induced cell cytotoxicity and oxidativestress in HepG2 cells. [6]-Gingerol pretreatment attenuated radiation-induced cell cytotoxicitycaused by 5Gy(half lethal dose, LD50of HepG2 cells). The measurements of superoxide dismutase(SOD) and catalase(CAT) activity were also performed. The results showed that [6]-gingerol pre-treatment reduced increasing SOD and CAT activity after exposure of IR, indicating that [6]-gin-gerol protected oxidative stress by regulating cellular antioxidant enzyme(SOD and CAT) activity.These findings suggest that [6]-gingerol acts as a radioprotector by attenuating cell cytotoxicityand oxidative stress.