In a pre-clinical meta-analysis of gingerol compounds anticancer, anti-inflammatory, anti-fungal, antioxidant, neuroprotective and gastroprotective properties were reported, which include studies in-vitro and in-vivo.
A few in-vivo studies have proposed that gingerols facilitate healthy glucose regulation for diabetics.
Many studies have been around the effects of gingerols on a wide range of cancers including leukemia, prostate, breast, skin, ovarian, lung, pancreatic and colorectal.
There has not been much clinical testing to observe gingerols physiological impacts in humans.

While many of the chemical mechanisms associated with the effects of gingerols on cells have been thoroughly studied, few have been in a clinical setting.
This is due to the high variability in natural phytochemicals and the lack of efficacy in research.
Most herbal medicine, which include gingerols, are under the restrictions of the Food and Drug Administration in the United States and experimental methods have not held up to scrutiny which has decreased the value in phytochemical research.
Herbal medicine is untested for quality assurance, potency and effectiveness in clinical settings due to a lack of funding in eastern medical research.
Most research on [6]-Gingerol has been on either mouse subjects (in-vivo) or on cultured human tissue (in-vitro) and may be used in the future to discuss possible applications for multi-target disease control.

An investigation scrutinizing gingerol's anti-fungal capabilities remarked that an African species of ginger tested higher in both gingerol and shogaol compounds than the more commonly cultivated Indonesian relative.
When tested for the anti-fungal properties the African ginger combated against 13 human pathogens and was three times more effective than the commercial Indonesian counterpart.
It is thought that gingerol compounds work in tandem with the other phytochemicals present including shogaols, paradols and zingerone.

In a meta analysis looking at many different phytochemical effects on prostate cancer, two specific studies using mice observed [6]-gingerol compounds induced apoptosis in cancer cells by interfering with the mitochondrial membrane.
There were also observed mechanisms associated with the disruption of G1 phase proteins to stop the reproduction of cancer cells which is also an associated benefit of other relevant anticancer studies.
The main mechanism by which gingerol phytochemicals act on cancer cells seems to be protein disruption.
The anti-carcinogenic activity of [6]-gingerol and [6]-paradol was analysed in a study observing the cellular mechanisms associated with mouse skin cancer which targeted the activator proteins associated with tumor initiation.
Gingerol compounds inhibited the transformation of normal cells into cancer cells by blocking AP-1 proteins and when cancer did develop paradol encouraged apoptosis due to its cytotoxic activity. [
6]-Gingerol exhibits cell cycle arrest capabilities, apoptotic action and enzyme-coupled cell signaling receptor degradation in cancer cells.
Gingerol has been observed to stop proliferation through inhibiting the translation of Cyclin proteins necessary for replication during G1 and G2 phase of cell division.
To promote apoptosis in cancer cells Cytochrome C is ejected from the mitochondria which ceases ATP production leaving a dysfunctional mitochondria.
The Cytochrome C assembles an apoptosome which activates the Caspase-9 and initiates an executioner Caspase cascade, effectively breaking down DNA into histones and promoting apoptosis. [
6]-Gingerol also inhibits the anti-apoptotic Bcl-2 proteins on the surface of mitochondria, which in turn increases the capabilities for the pro-apoptotic Bcl-2 proteins to initiate cell death.
Cancer cells exhibit high amounts of growth hormone activator proteins that are expressed through enzyme-coupled signaling pathways.
By halting the phosphorylation of PI-3-Kinase the Akt protein cannot bind with its PH domain, effectively deactivating the downstream signal.
Successively keeping Bad proteins bound to
In a pre-clinical meta-analysis of gingerol compounds anticancer, anti-inflammatory, anti-fungal, antioxidant, neuroprotective and gastroprotective properties were reported, which include studies in-vitro and in-vivo. A few in-vivo studies have proposed that gingerols facilitate healthy glucose regulation for diabetics. Many studies have been around the effects of gingerols on a wide range of cancers including leukemia, prostate, breast, skin, ovarian, lung, pancreatic and colorectal. There has not been much clinical testing to observe gingerols physiological impacts in humans.
While many of the chemical mechanisms associated with the effects of gingerols on cells have been thoroughly studied, few have been in a clinical setting. This is due to the high variability in natural phytochemicals and the lack of efficacy in research. Most herbal medicine, which include gingerols, are under the restrictions of the Food and Drug Administration in the United States and experimental methods have not held up to scrutiny which has decreased the value in phytochemical research. Herbal medicine is untested for quality assurance, potency and effectiveness in clinical settings due to a lack of funding in eastern medical research. Most research on [6]-Gingerol has been on either mouse subjects (in-vivo) or on cultured human tissue (in-vitro) and may be used in the future to discuss possible applications for multi-target disease control.
An investigation scrutinizing gingerol's anti-fungal capabilities remarked that an African species of ginger tested higher in both gingerol and shogaol compounds than the more commonly cultivated Indonesian relative. When tested for the anti-fungal properties the African ginger combated against 13 human pathogens and was three times more effective than the commercial Indonesian counterpart. It is thought that gingerol compounds work in tandem with the other phytochemicals present including shogaols, paradols and zingerone.
In a meta analysis looking at many different phytochemical effects on prostate cancer, two specific studies using mice observed [6]-gingerol compounds induced apoptosis in cancer cells by interfering with the mitochondrial membrane. There were also observed mechanisms associated with the disruption of G1 phase proteins to stop the reproduction of cancer cells which is also an associated benefit of other relevant anticancer studies. The main mechanism by which gingerol phytochemicals act on cancer cells seems to be protein disruption. The anti-carcinogenic activity of [6]-gingerol and [6]-paradol was analysed in a study observing the cellular mechanisms associated with mouse skin cancer which targeted the activator proteins associated with tumor initiation. Gingerol compounds inhibited the transformation of normal cells into cancer cells by blocking AP-1 proteins and when cancer did develop paradol encouraged apoptosis due to its cytotoxic activity. [6]-Gingerol exhibits cell cycle arrest capabilities, apoptotic action and enzyme-coupled cell signaling receptor degradation in cancer cells. Gingerol has been observed to stop proliferation through inhibiting the translation of Cyclin proteins necessary for replication during G1 and G2 phase of cell division. To promote apoptosis in cancer cells Cytochrome C is ejected from the mitochondria which ceases ATP production leaving a dysfunctional mitochondria. The Cytochrome C assembles an apoptosome which activates the Caspase-9 and initiates an executioner Caspase cascade, effectively breaking down DNA into histones and promoting apoptosis. [6]-Gingerol also inhibits the anti-apoptotic Bcl-2 proteins on the surface of mitochondria, which in turn increases the capabilities for the pro-apoptotic Bcl-2 proteins to initiate cell death. Cancer cells exhibit high amounts of growth hormone activator proteins that are expressed through enzyme-coupled signaling pathways. By halting the phosphorylation of PI-3-Kinase the Akt protein cannot bind with its PH domain, effectively deactivating the downstream signal. Successively keeping Bad proteins bound to
Gingerol