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is oxidative stress, as explained by diabetic status (Han et al., 2015). Priscilla et al. (2015)

further, documented that high fat diet fed in streptozotocin-induced diabetic rats caused
inflammation and necrosis in the liver, indicated by the increased levels of liver function

markers in serum, while NG supplementation restored these altered enzymes to normalcy.
NG supplementation has been found to hamper the expression of proinflammatory mediators

and protect liver against oxidative damage via NF-κB down regulation (Chtourou et al.,
2015). NG has also shown to play an important role in protection against lead and arsenic

induced renal damage. The antioxidant activity of NG may be accounted for this phenomenon

(Wang et al., 2012). Kapoor and Kakkar et al. (2014) investigated the protective effect of NG
on hepatopathy in streptozotocin induced diabetic rats. They demonstrated altered activities

of antioxidant enzymes, liver and kidney marker enzymes and carbohydrate metabolizing

enzymes, MDA formation and production of ROS, and activation of caspase 9/3 leading to
apoptosis (mitochondrial apoptotic pathway) of liver tissue and DNA damage, as diabetic

complications induced by streptozotocin in rats. NG supplementation prevented oxidative
stress and apoptotic events, thus exerting antihyperglycemic effects against diabetes-induced

liver damage and indicating the beneficial effects of NG for the management of diabetic
hepatopathy.

4.6. Anticarcinogenic ability

Several in vivo and in vitro studies have reported the anticarcinogenic and

antimutagenic activity of NG (Krishnakumar et al., 2011). In tumour progression,
angiogenesis plays a major role, and therefore a great deal of attention has been drawn

towards using antiangiogenic therapy generally having low toxicity in cancer therapeutics
(Folkman, 1995). NG has also been reported to possess antiangiogenic properties (Qin et al.,

2011), which may be attributed to its role in reduction of various angiogenic factors, e.g.
vascular endothelial growth factor in human tumour cell lines (Schindler and Mentlein,

2006). Tumour growth attenuation has been observed by many researchers in various

systemic malignancies (Kapoor and Kakkar, 2014). For instance, NG decreased tumour
growth in N-methyl-Nʹ-nitro-N nitrosoguanidine-induced gastric carcinoma by inducing

redox activity in tumour cells (Ekambaram et al., 2008) and in NDEA-induced hepato-
cellular carcinoma by inhibiting NF-κB activity within the tumour cells and altering Bcl-

2/Bax ratio (Subramanian and Arul, 2012). Anand et al. (2012) demonstrated the
angioinhibitory activity of NG along with curcumin using chorioallantoic membrane (CAM)

assay and in vivo Ehrlich Ascites Carcinoma (EAC) model and also reported the

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