Dr. Weeks’ Comment: Got liver cancer? Take it seriously and detox with “the billion cleaning ladies who scrub your cell membranes” and eat the most concentrated greens product with milk thistle seeds, then follow the principles of Corrective Cancer Care and eat whole crushed black cumin seed – the Seeds of Eden. And drink plenty of good quality water.
In Vitro Challenge using Thymoquinone on Hepatocellular Carcinoma (HepG2) Cell Line
SOURCE Iranian Journal of Pharmaceutical Research Article 7, Volume 7, Number 4, Autumn 2008, Page 283-290
Authors: Hassan, et al
lack seed (Nigella sativa) is considered as a biological response modifier. Thymoquinone (TQ) is the bioactive and the most abundant constituent of the volatile oil of this seed which has been shown to possess anti-inflammatory, antioxidant and anti-neoplastic effects… TQ ability to induced apoptosis was determined by Flowcytometry and colorimetric measurement of Caspases 3 and 9. The apoptotic effect of TQ was much more dramatic after 12 h treatment and the activity of Caspases 3 and 9 was increased… It could be concluded that Thymoquinone is a promising anti-cancer agent for hepatocellular carcinoma.
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Thymoquinone suppression of the human hepatocellular carcinoma cell growth involves inhibition of IL-8 expression, elevated levels of TRAIL receptors, oxidative stress and apoptosis
- Ashour, A.E., Abd-Allah, A.R., Korashy, H.M. et al. Mol Cell Biochem (2014) 389: 85. doi:10.1007/s11010-013-1930-1
Abstract
Hepatocellular carcinoma (HCC) is the fourth most common solid tumor worldwide. The chemokine interleukin-8 (IL-8) is overexpressed in HCC and is a potential target for therapy. Although the transcription factor NF-κB regulates IL-8 expression, and while thymoquinone (TQ; the most bioactive constituent of black seed oil) inhibits NF-κB activity, the precise mechanisms by which TQ regulates IL-8 and cancer cell growth remain to be clarified. Here, we report that TQ inhibited growth of HCC cells in a dose- and time-dependent manner, caused G2M cell cycle arrest, and stimulated apoptosis. Apoptosis was substantiated by activation of caspase-3 and -9, as well as cleavage of poly(ADP-ribose)polymerase. TQ treatments inhibited expression of NF-κB and suppressed IL-8 and its receptors. TQ treatments caused increased levels of reactive oxygen species (ROS) and mRNAs of oxidative stress-related genes, NQO1 and HO-1. Pretreatment of HepG2 cells with N-acetylcysteine, a scavenger of ROS, prevented TQ-induced cell death. TQ treatment stimulated mRNA expression of pro-apoptotic Bcl-xS and TRAIL death receptors, and inhibited expression of the anti-apoptotic gene Bcl-2. TQ enhanced TRAIL-induced death of HepG2 cells, in part by up-regulating TRAIL death receptors, inhibiting NF-κB and IL-8 and stimulating apoptosis. Altogether, these findings provide insights into the pleiotropic molecular mechanisms of TQ-dependent suppression of HCC cell growth and underscore potential of this compound as anti-HCC drug.