GINGERGinger (Zingiber officinale) is a member of the Zingiberaceae family and is consumed widely not only as a spice but also as a medicinal agent (see also Chapter 7 on ginger). Other members of the family include turmeric and cardamom. Ginger’s cultivation appears to have begun in South Asia and has now spread to various parts of the world. It is sometimes called “root ginger” to distinguish it from other products that share the name. The principal constituents of ginger include -gingerol, -paradol, -shogaol (dehydration gingerols), and zingerone. Several studies have investigated ginger’s antioxidant properties (Chrubasik, Pittler, and Roufogalis 2005). Gingerol has also been shown to decrease intracellular ROS formation in human keratinocyte cells (Kim et al. 2007), inhibit angiogenesis in human ECs, and limit nitrogen oxide synthase expression and epidermal growth factor-induced cell transformation and AP-1 transcriptional complexes in JB6 cells (Bode et al. 2001; Ippoushi et al. 2003; Davies et al. 2005; Kim et al. 2005).
Feeding NIN/Wistar rats a diet containing up to 0.5-5% ginger for 1 month significantly increased (p < .05) several liver antioxidant enzymes, including superoxide dismutase (76–141%), catalase (37–94%), and GPx (11–30%; Kota, Krishna, and Polasa 2008). Lipid and protein oxidation was inhibited in rats consuming ginger, as evidenced by significant decreases (p < .05) in liver and kidney levels of MDA (35-59% and 27-59%, respectively) and carbonyl levels (23-36%), compared to controls (Kota, Krishna, and Polasa 2008). Ippoushi et al. (2007) found that AIN-76 basal diets with 2% ginger decreased TBARS by 29% (p < .05) and suppressed 8-hydroxy-2′-deoxyguanosine (8-OHdG, a product of oxidative DNA damage) levels in Wistar rats. TBARS was also significantly decreased (p < .001) in Wistar rats fed with diets supplemented with 1% ginger following exposure to lindane, a pesticide that is a global pollutant, (Ahmed et al. 2008).
Various animal models have been used to examine the role of ginger in cancer prevention. For example, Ihlaseh et al. (2006) exposed male Wistar rats to N-butyl-N-(4-hydroxybutyl)-nitrosamine (BNN) and uracil salt to induce tumors resembling human low-grade papillary urothelial neoplasia. Rats fed with a basal diet supplemented with 1% ginger extract for 26 weeks had significantly fewer urothelial lesions compared to the controls or those fed with the diet with 0.5% ginger (p = .013; Ihlaseh et al. 2006). However, ginger does not appear effective in all cases, as evidenced by the lack of protection against proliferative lesions in the bladders of Swiss mice fed with a 1% or 2% extract and exposed to BNN/N-methyl-N-nitrosourea (Bidinotto et al. 2006).
Induction of phase I and II activities may partially account for ginger’s anticarcinogenic actions. Banerjee et al. (1994)found that providing 10-μL ginger oil daily for 2 weeks to Swiss mice increased aryl hydrocarbon hydroxylase activity about 25% (p < .05) and increased GST by 60% (p < .01). No significant increase in GST induction was observed in Swiss mice fed with 160 mg ginger/gram diet (Aruna and Sivaramakrishnan 1990).
Inflammation is a significant risk factor for cancer, including prostate cancer. Mitogen-activated protein kinase phosphatase-5 (MKP5) is implicated as a proinflammatory inhibitor in innate and adaptive immune response in vivo (Zhang et al. 2004). Providing -gingerol upregulated MKP5 expression in normal prostate epithelial cells treated with 50 μM gingerol; likewise, it upregulated MKP5 expression in human prostate cancer cell lines (DU145, PC-3, LNCaP and LAPC-4; Nonn, Duong, and Peehl 2007). Ginger extracts, more so than their individual components, have been shown to inhibit lipopolysaccharide-induced prostaglandin E2 (PGE2) production to an extent similar to that of indomethacin, a nonsteroidal anti-inflammatory drug. Subfractions of ginger extract decreased LPS-induced COX-2 mRNA expression levels, although apparently not through the nuclear factor κB (NF-κβ) or activating protein 1 (AP-1) transcription factor pathways, because the ginger extracts did not inhibit TNF-α production (Lantz et al. 2007). -paradol, another active compound in ginger, is reported to induce apoptosis in human promyelocytic leukemia cells, JB6 cells, an oral squamous carcinoma cell line, and Jurkat human T-cell leukemia cells in a dosedependent manner (Huang, Ma, and Dong 1996; Lee and Surh 1998; Keum et al. 2002; Miyoshi et al. 2003). It is unclear whether -paradol has molecular targets similar to -gingerol.
Ginger also appears to have antitumorigenic properties. Several cell lines have been examined for their sensitivity to ginger. For example, alcoholic extracts of ginger inhibited tumor cell growth for Dalton’s lymphocytic ascites tumor cells and human lymphocytes at concentrations of 0.2-1 mg/mL in vitro (Unnikrishnan and Kuttan 1988). In a study of cytotoxic activities of several compounds in ginger against four tumor cell lines (A549, human lung cancer; SK-OV-3, human ovarian cancer; SK-MEL-2, human skin cancer; and HCT-15, human colon cancer), -shogaol was the most potent (ED50: 1.05–1.76 μg/mL), and -, -, -, and -gingerol displayed moderate cytotoxicity (ED50: 4.92-30.05; Kim et al. 2008). Adding -gingerol (25 μM) has been reported to inhibit proliferation in rat ascites hepatoma cells AH109A and increase apoptosis at higher concentrations (50 μM; Yagihashi, Miura, and Yagasaki 2008). Likewise, adding -shogoal (60 μM) to COLO295 cells has been reported to increase the expression of GADD153, a gene that promotes apoptosis (Chen et al. 2007). -shogaol (>50 μM) also provokes DNA damage and apoptosis through an oxidative stressmediated caspase-dependent pathway (Chen et al. 2007). Similarly, incubation of HEp-2 cells with ginger (250 μg/mL, 500 μg/mL, or 1000 μg/mL) resulted in a dose-dependent decrease in nitrite generation, increased production of superoxide, and decreased GSH levels compared to untreated cells, indicating ginger-induced apoptosis through the generation of ROS (Chen et al. 2007).
Ginger is also recognized for its potential usefulness to reduce nausea. To determine whether ginger had antiemetic effects in cisplatin-induced emesis, Manusirivithaya et al. (2004) conducted a randomized, double-blinded, crossover study in 48 gynecologic cancer patients. The addition of ginger (1 g/day) to a standard antiemetic regimen has no advantage in reducing nausea or vomiting in the acute phase of cisplatin-induced emesis. In the delayed phase, ginger and metoclopramide have no statistically significant difference in efficacy (Manusirivithaya et al. 2004). In another study, 1000 mg of ginger was compared to 20-mg intravenous (IV) metoclopramide, and to 4-mg IV ondansetron in controlling nausea in patients receiving cyclophosphamide chemotherapy. Ginger was determined to be as effective as metoclopramide, but neither was as effective as ondansetron (Sontakke, Thawani, and Naik 2003).
Overall, while the anticancer findings of ginger are intriguing and several processes may be associated with the observed responses, additional studies are needed to clarify the underlying mechanisms and to determine overall benefits to humans (Pan et al. 2008).
Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
drsnojha@rediffmail. com - See more at: http://infoayushdarpan.blogspot.in/2016/02/salient-features-of-amlapitta.html#sthash.AP6bCKCS.dpuf