Nigella sativa extract kills pre-malignant and malignant oral squamous cell carcinoma cells.

In this study, the potential of Nigella sativa was evaluated in the management of oral cancer through assays designed to mimic conditions expected when chewing the whole seeds or use of a seed extract. For this purpose, a water-based extract of N. sativa seeds was prepared, mimicking the chewing process. This extract demonstrated significant cytotoxic effect on oral cancer and pre-cancerous leukoplakia cells in vitro at a much lower concentration than the predicted oral concentration that could be achieved upon seed chewing. When the active constituent(s) in this water-based N. sativa seed extract, was explored significant quantities of the compound α-hederin was detected but only modest quantities of thymoquinone suggesting that thymoquinone is not fully released into the aqueous medium during the chewing process. While the N. sativa seed extract induced a different effect on the cells than that of pure thymoquinone, α-hederin alone induced a very similar effect on the cells to that of the extract. These results suggest that α-hederin and not thymoquinone, is the major component of the seed that is responsible for the inhibitory effect observed in vitro. Therefore, chewing N. sativa whole seeds or applying a concentrated extract on the oral lesions may be an inexpensive, widely available, and effective option for patients at risk of developing oral cancer who are receiving no other preventive treatment.

Histone deacetylase inhibitors induce antigen specific anergy in lymphocytes: a comparative study.

Induction of immune tolerance to transplanted tissue continues to be a challenge for organ transplantation. In the present study, six widely used histone deacetylase inhibitors (HDAI), sodium butyrate (n-butyrate), Trichostatin A, Oxamflatin, Scriptaid, HDAC I and HDAC III, were examined for ability to induce antigen-specific immune anergy in cloned and naïve murine CD4(+) T cells. When first compared for their ability to inhibit histone deacetylation Trichostatin A was found to be 10 times more potent than HDAC III, Oxamflatin and Scriptaid and 10(4) times more potent than n-butyrate. When we compared ability to inhibit CD4(+) T cell proliferation in response to IL-2 stimulation, Trichostatin A was the most potent with 100% inhibition using 100 nM Trichostatin A, while 1 muM of HDAC III, Oxamflatin and Scriptaid and 1 mM of n-butyrate were required for this effect. When the tolerogenic activity of Trichostatin A, Scriptaid and n-butyrate were compared using cloned Th1 cells specific for keyhole limpet hemocyanin (KLH), all three HDAI were effective, but Trichostatin A was again the most potent. Finally, Trichostatin A (0.05 mM) was shown to induce anergy in OT-II ovalbumin-specific naïve CD4(+) T-cells. We concluded that Trichostatin A was the most potent HDAI with regard to inhibition of histone deacetylation and the ability to induce antigen-specific anergy in both cloned and naïve CD4(+) T cells. These results will guide future studies examining HDAIs for ability to induce clinical tolerance in organ transplantation.