Имбирьдің құрамындағы джинджерол: қасиеттері мен зерттеулер

Gingerol ([6] gingerol) is a phenolic phytochemical compound found in fresh ginger that activates heat receptors on the tongue. It is normally found as a pungent yellow oil in the ginger rhizome, but can also form a low melting crystalline solid. This chemical compound is found in all members of the Zingiberaceae family and is high in concentrations in the grains of paradise as well as an African Ginger species. Cooking ginger transforms gingerol via a reverse aldol reaction into zingerone, which is less pungent and has a spicy sweet aroma. When ginger is dried or mildly heated, gingerol undergoes a dehydration reaction forming shogaols, which are about twice as pungent as gingerol. This explains why dried ginger is more pungent than fresh ginger. Ginger also contains [8] gingerol, [10] gingerol, and [12] gingerol, collectively deemed gingerols.

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. 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 anti apoptotic proteins which keeps them from promoting cell growth, consequently, a double negative cellular signaling pathway to promote apoptosis. Cultured human breast cancer cells were subjected to various concentrations of [6] gingerol to determine the impacts on live cells. These concentration dependent results concluded that there was no impact at 5 μM but a reduction of 16% occurred at 10 μM. [6] gingerol improved glutathione production in dose dependent results which suggested that the higher a dosage the more of an effect [6] gingerol had. There are some pro oxidant behaviors to gingerol compounds when the concentration reaches high levels although also considered, in normal conditions these phytochemicals observed have anti inflammatory and anti oxidant qualities.

Both ginger (Zingiber officinale) and turmeric (Curcuma longa) had been suspected to utilize phenylpropanoid pathway and produce putative type III polyketide synthase products based on the research of 6 gingerol biosynthesis by Denniff and Whiting in 1976 and by Schröder's research in 1997. 6 Gingerol is the major gingerol in ginger rhizomes and it possesses some interesting pharmacological activities like analgesic effect. While the biosynthesis of 6 gingerol is not fully elucidated, plausible pathways are presented here. In the proposed biosynthetic pathway, Scheme 1, L Phe (1) is used as the starting material. It is converted into Cinnamic acid (2) via phenylalanine ammonia lyase (PAL). Then it is turned into p Coumaric acid (3) with use of cinnamate 4 hydroxylase (C4H). 4 coumarate:CoA ligase (4CL) is then used to get p Coumaroyl CoA (5). P Coumaroyl shikimate transferase (CST) is the enzyme that is responsible for the bonding of shikimic acid and p Coumaroyl CoA. The complexed (5) is then selectively oxidized at C3 by p coumaroyl 5 O shikimate 3' hydroxylase (CS3'H) to alcohol. With another action of CST, shikimate is broken off from this intermediate, thereby yielding Caffeoyl CoA (7). In order to get desired substitution pattern on the aromatic ring, caffeoyl CoA O methyltransferase (CCOMT) converts the hydroxyl group at C3 into methoxy as seen in Feruloyl CoA (8). Up until this step, according to Ramirez Ahumada et al., the enzyme activities are very active. It is speculated that some polyketide synthases (PKS) and reductases are involved in final synthesis of 6 Gingerol (10). Because it is unclear whether the methoxy group addition is performed before or after the condensation step of the polyketide synthase, alternative pathway is shown in Scheme 2, where methoxy group is introduced after PKS activity. In this alternative pathway, the enzymes involved are likely to be cytochrome p450 hydroxylases, and S adenosyl L methionine dependent O methyltransferases (OMT). There are three possibilities for the reduction step by Reductase: directly after PKS activity, after PKS and Hydroxylase activity, or in the end after PKS, Hydroxylase, and OMT activity.