Description: |
10-Gingerol has anti-cancer, anti-neuroinflammatory, and anti-bacterial effects, it effectively inhibits the growth of the oral pathogens, and inhibits exogenous ghrelin deacylation.10-Gingerol induces [Ca2+]i rise by causing Ca2+ release from the endoplasmic reticulum and Ca2+ influx from non-L-type Ca2+ channels in SW480 cancer cells.10-Gingerol-induced apoptosis was accompanied by phosphorylation of the mitogen-activated protein kinase (MAPKs) family, c-Jun N-terminal kinase (JNK), p38 MAPK (p38), and extracellular signal-regulated kinase (ERK). |
Targets: |
JNK | p38MAPK | ERK | Calcium Channel | Bcl-2/Bax | NF-kB | IL Receptor | TNF-α | Akt |
In vitro: |
Food Chem. 2013 Dec 1;141(3):3183-91. | Anti-neuroinflammatory capacity of fresh ginger is attributed mainly to 10-gingerol.[Pubmed: 23871076] | Despite the anti-neuroinflammatory capacity of ginger, the corresponding active constituents are unclear. METHODS AND RESULTS: This study analyzed the composition of fresh ginger ethanolic extract by using LC-MS. Inhibitory activities of fresh ginger extract and seven gingerol-related compounds on the neuro-inflammation were also evaluated by using a lipopolysaccharide (LPS)-activated BV2 microglia culture model. Except for zingerone and 6-gingerol, other gingerols and shogaols at a concentration of 20 μM inhibited the production of nitric oxide, IL-1β, IL-6 and TNF-α as well as their mRNA levels in LPS-activated BV2 microglia. Blocking NF-κB activation was the underlying mechanism responsible for inhibiting the proinflammatory gene expression. Increasing the alkyl chain length enhanced the anti-neuroinflammatory capacity of gingerols yet, conversely, attenuated those of shogaols. 6-Gingerol was the most abundant compound in the fresh ginger extract, followed by 10-Gingerol. Furthermore, fresh ginger extract exhibited a significant anti-neuroinflammatory capacity, which was largely owing to 10-Gingerol, but not 6-gingerol. |
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In vivo: |
Biochem Biophys Res Commun. 2011 Sep 2;412(3):506-11. | 10-Gingerol, a component of rikkunshito, improves cisplatin-induced anorexia by inhibiting acylated ghrelin degradation.[Pubmed: 21846463] | Rikkunshito (RKT), a Japanese traditional medicine, has been shown to stimulate food intake in rats with cisplatin-induced anorexia; however, the underlying mechanisms remain unknown. METHODS AND RESULTS: In this study, we investigated whether RKT is involved in the degradation of peripheral ghrelin. RKT inhibited decreases in plasma ghrelin level and enhanced acyl- to desacyl-ghrelin (A/D) ratio in cisplatin-treated rats. Several components of RKT demonstrated inhibitory activity against ghrelin deacylating enzymes. In addition, 10-Gingerol, a component of RKT, inhibited exogenous ghrelin deacylation. CONCLUSIONS: Therefore, RKT may enhance plasma acyl-ghrelin level, at least in part, by inhibiting the circulating ghrelin degrading enzyme. |
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