Effect of TTRAP expression on apoptosis induced by hydroquinone in HL-60 cells in vitro / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effect of TTRAP expression on apoptosis induced by hydroquinone in HL-60 cells in vitro, and explore the relationship between TTRAP expression and the apoptosis.</p><p><b>METHODS</b>Apoptotic and necrotic rate was examined by flow cytometer with Anti-AnnexinV/FITC Plus PI staining. The mRNA expression of TTRAP was detected by RT-PCR. The differences in different treated groups were compared.</p><p><b>RESULTS</b>After different concentrations of hydroquinone to the cells for 0, 4, 8, 12 h culture, were added, the cell apoptotic rate in different concentrations of hydroquinone groups was significantly higher than that in blank control groups. The optimal concentration of hydroquinone was 200 micromol/L, lasting for 8 h. When it was 250 micromol/L, the necrotic rate increased significantly. The apoptosis induced by hydroquinone was associated with the culture time at the concentration of 200 micromol/L, and the peak apoptotic time was 8 h. Then the apoptotic rate decreased and necrotic rate increased. Furthermore, with the concentrations of hydroquinone increased and time lasted for 8 h, the apoptotic rate of cells increased, the amount of TTRAP expression in the mRNA level also increased accordingly. When the concentrations of hydroquinone was above 250 micromol/L, necrotic rate increased sharply, and the amount of TTRAP expression decreased.</p><p><b>CONCLUSION</b>Hydroquinone could induce apoptosis of HL-60 cells. The up-regulation of TTRAP expression may promote hydroquinone to induce HL-60 cells to go into apoptosis in vitro with dose-effect and time-effect relationship.</p>

Redox modulation of large conductance calcium-activated potassium channels in rat cultured trigeminal ganglion neurons / 中国应用生理学杂志

<p><b>AIM</b>To observe redox modulation of ion channel in trigeminal ganglion neurons by oxidants and reducing agents.</p><p><b>METHODS</b>The effects of oxidants and reducing agents on maxi-conductance calcium-activated potassium channel in cultured rat trigeminal ganglion neurons by using whole-cell patch-clamp technique.</p><p><b>RESULTS</b>Methionine-specific oxidant chloramine-T (Ch-T) 1 mmol/L slightly increased the current amplitude and this enhancement did not antagonized by DTT. In contrast, cysteine-specific reagent 5, 5'-dithio-bis(2-nitrobenzoic acid) (DTNB) 500 micromol/L significantly decreased current amplitude of BK(Ca) channels. The effect was reversed by the reducing agent 2 mmol/L 1, 4-dithio-DL-threitol (DTT).</p><p><b>CONCLUSION</b>Reactive oxygen species were definitely involved in regulation of native neuronal function via redox modulation of BK(Ca) channels, which are suggested to play compensatory roles under oxidative stress-related conditions.</p>