Diosgenin is a major bioactive constituent of various edible pulses and roots, well characterized in the seeds of fenugreek as well as in the root tubers of wild yams. The findings from pre-clinical and mechanistic studies strongly implicate the use of diosgenin as a novel multi-target based chemo preventive or therapeutic agent against several chronic diseases. Diosgenin has been shown to increase cholesterol secretion fiveto seven-fold in the bile of rats without altering the output of bile salts and phospholipids (Kosters et al., 2005; Nervi et al., 1988; Nibbering et al., 2001). Recently, it was shown that the biliary cholesterol secretion stimulated by diosgenin and leading to fecal cholesterol excretion is independent of intestinal cholesterol absorption. The anti-cancer effects of diosgenin in vitro through different mechanisms was investigated and was shown that it could use in the treatment Colon cancer, breast cancer, prostate cancer and some others. Also was investigates the effect of diosgenin on hepatitis C virus (HCV) replication and was shown that compound can inhibits HCV replication at low µM concentrations. Diosgenin was able to protect the kidney from morphological changes associated with ovariectomy. The mechanism is responsible for this protection was the conversion of diosgenin to progesterone. The extensive pre-clinical and clinical research should be carried out prior to advocating the safe and efficacious use of diosgenin and diosgenin-rich plant extracts against the prevention and control of diseases.

Camphene is a bicyclic monoterpene, a Plant Derived Monoterpene, which possessed antitumor activity. This was found in vivo by inhibiting subcutaneous tumor growth of highly aggressive melanoma cells in a syngeneic model, suggesting a promising role of this compound in cancer therapy. In addition was shown, that camphene lowered cholesterol and triglycerides (TG) in the plasma of hyperlipidemic rats without affecting HMG-CoA reductase activity. And was suggested, that camphene upregulated Sterol regulatory element-binding proteins (SREBP-1) expression and microsomal triglyceride transfer protein (MTP) inhibition was likely to be a probable mechanism whereby camphene exerts its hypolipidemic effect.