Trichostatin (TSA) as a reason inhibitor can adjust many biological properties including the cell apoptosis and cell proliferation in all kinds of cancer cells. Here, we evaluate the effects of TSA in growth and death sheila cervical cancer cells and reactive oxygen species (ROS) and glutathione (GSH) content. Dose - and the time to observe somatostatin in hella cells and a IC50 about 20 nM 72 h. The agency also induced apoptosis cells die, as annexin v bovine serum albumin dyed cells, caspase 3 activation and the loss of mitochondrial membrane potential (MMP; ∆ ψ m). In addition, the government of the base class library 2 small interference RNA aggravate tsa induced hela cell death. All the testing caspase inhibitor greatly save some cell tsa induced hela cell death. TSA increased, O2 - level and inducing glutathione hella cell. Caspase inhibitor decreased obviously, O2 - level, GSH hella cell tsa treatment. In addition, n-acetyl cysteine (NAC; a known antioxidant) significantly prevent cell death and glutathione tsa treatment of hella cells, by reducing the O2 - level. In short, TSA cytostatic sheila through the BCL 2 mediated apoptosis closely related, O2,, glutathione levels.

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