10-Gingerol CAS NO.23513-15-7

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
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Chemical Properties of 10-Gingerol

Source of 10-Gingerol

The rhizomes of Zingiber officinale Roscoe.

Biological Activity of 10-Gingerol

Protocol of 10-Gingerol

Preparing Stock Solutions of 10-Gingerol

References on 10-Gingerol

Anti-neuroinflammatory capacity of fresh ginger is attributed mainly to 10-gingerol.[Pubmed:23871076]

Food Chem. 2013 Dec 1;141(3):3183-91.

Despite the anti-neuroinflammatory capacity of ginger, the corresponding active constituents are unclear. 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 muM inhibited the production of nitric oxide, IL-1beta, IL-6 and TNF-alpha as well as their mRNA levels in LPS-activated BV2 microglia. Blocking NF-kappaB 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.

10-Gingerol, a component of rikkunshito, improves cisplatin-induced anorexia by inhibiting acylated ghrelin degradation.[Pubmed:21846463]

Biochem Biophys Res Commun. 2011 Sep 2;412(3):506-11.

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. 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. Therefore, RKT may enhance plasma acyl-ghrelin level, at least in part, by inhibiting the circulating ghrelin degrading enzyme.

[10]-Gingerol induces mitochondrial apoptosis through activation of MAPK pathway in HCT116 human colon cancer cells.[Pubmed:25148824]

In Vitro Cell Dev Biol Anim. 2015 Jan;51(1):92-101.

The present study was designed to investigate the molecular mechanisms of [10]-gingerol activity against HCT116 human colon cancer cells. [10]-Gingerol inhibited the proliferation of HCT116 cells by 50% at a concentration of 30 muM, and this inhibition was dose-dependent accompanied by the morphological changes indicative of apoptosis. Furthermore, flow cytometric analysis showed that [10]-gingerol increased DNA in the sub-G1 phase of the cell cycle, and the extent of apoptosis was confirmed by Annexin V and PI double staining. Analysis of the mechanism of these events indicated that [10]-gingerol-treated cells exhibited an increased ratio of Bax/Bcl-2, resulting in the activation of caspase-9, caspase-3, and poly-ADP-ribose polymerase in a dose-dependent manner, which are hallmarks of apoptosis. Moreover, [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). This is the first report to demonstrate the cytotoxic effect of [10]-gingerol on human colon cancer cells, as well as the first to describe its possible chemotherapeutic potentials.

10-Gingerol inhibits proliferation and invasion of MDA-MB-231 breast cancer cells through suppression of Akt and p38MAPK activity.[Pubmed:26554741]

Oncol Rep. 2016 Feb;35(2):779-84.

In the present study, we investigated the roles and molecular mechanism of 10-Gingerol, a phenolic compound isolated from Zingiber officinale, in regulating cell proliferation and invasion of MDAMB231 breast cancer cells. 10-Gingerol treatment inhibited cell proliferation through downregulation of cell cycle regulatory proteins such as cyclin-dependent kinases and cyclins, and subsequent induction of G1 phase arrest. In addition, 10gingerol treatment blocked cell invasion in response to mitogenic stimulation. These antitumor activities of 10gingerol were mediated through inactivation of Akt and p38MAPK activity, and suppression of epidermal growth factor receptor expression. Collectively, these findings demonstrate the pharmacological roles of 10-Gingerol in regulating breast cancer cell growth and progression, and suggest further evaluation and development as a potential therapeutic agent for the prevention and treatment of breast cancer.

Description

10-Gingerol is a major pungent constituent in the ginger oleoresin from fresh rhizome, with anti-inflammatory, antioxidant and anti-proliferative activities. 10-Gingerol inhibits the proliferation of MDA-MB-231 tumor cell line with an IC50 of 12.1 μM.

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