The effect of p38 on the cycloheximide-induced HL-60 cell death through mitochondria pathway / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the effect of p38 on the cycloheximide (CHX)-induced HL-60 cell death through mitochondria pathway.</p><p><b>METHODS</b>Inhibition of p38 pathway was by SB203580 (SB). Four groups were set up: control, SB only, CHX only and SB + CHX. Sub-diploid cell ratio was detected by PI staining flow cytometry at 6, 9, 12, 18, 24 h time points, and apoptotic cell ratio by Annexin V-FITC/PI double staining flow cytometry at 6 h and 18 h time points. High J-aggregate cells were evaluated by the J-aggregate contents, measurement of the J-aggregate (FL2) and J-monomer (FL1) by JC-1 flow cytometry, calculation of the delta psi m by FL2/FL1 and analysis of the delta psi m changes at 18 h time points.</p><p><b>RESULTS</b>The sub-diploid cell ratio in CHX group was significantly higher than that in control group at 6 h time point, and the ratio in SB + CHX group was significantly higher than that in CHX group at 9 h time point. At 18 h time point the apoptotic cell ratios in both CHX and SB + CHX groups were significantly higher than those in control group (P < 0.01). There was no significant difference of apoptotic cell ratio between CHX group and SB + CHX group (P > 0.05). At 18 h time point the necrotic cell ratios in both CHX and SB + CHX groups were significantly higher than that in control group (P < 0.01); and that in SB + CHX group was significantly higher than that in CHX group (P < 0.01). The high J-aggregate cell ratios in CHX and SB + CHX groups were significantly lower than that in control group (P < 0.05), and that was signficantly lower in SB + CHX group than in CHX group (P < 0.01). For the FL2/FL1 value (delta psi m) CHX group (0.17 +/- 0.01) and SB + CHX group (0.05 +/- 0.003) were significantly higher than control group (0.38 +/- 0.02) (P < 0.01), and SB + CHX group was significantly lower than CHX group (P < 0.01).</p><p><b>CONCLUSION</b>CHX can induce HL-60 cell apoptosis and the cell mitochondria depolarization, and the latter was intensified by inhibition of the p38 pathway. p38 pathway may related to the cell necrosis in the cycloheximide-induced HL-60 cell apoptosis model. s</p>

Examination expression of CD3 and CD69 in nasal polyps / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the infiltration of T lymphocytes with CD3 expression as surface marker and the activation of T lymphocytes with CD69 expression as activation marker.</p><p><b>METHODS</b>Nasal polyp tissue samples and peripheral blood were obtained from 21 patients. The normal inferior turbinate mucosa and peripheral blood were obtained as comparison. Flow cytometry was adopted to detect the expression of CD3 and CD69 of T lymphocytes.</p><p><b>RESULTS</b>Nasal polyp tissue consisted of abundant T lymphocytes. Activation marker CD69 was expressed in T lymphocytes of nasal polyps (36.96 +/- 2.50)% and peripheral blood (4.66 +/- 0.18)% from the same patient. The expression rates of CD69 after a short-term stimulation (5 h) in response to PDB were (59.88 +/- 2.59)% and (92.76 +/- 0.55)% respectively. While T lymphocytes was rarely detected in normal inferior turbinate and the expression of CD69 was low in peripheral blood from normal human but almost all T lymphocytes were activated after stimulation.</p><p><b>CONCLUSIONS</b>There were generous of T lymphocytes infiltrating in nasal polyps. The expression of CD69 in T lymphocytes was abnormally high, which indicated that T lymphocytes infiltrating in nasal polyps were in activated state immunologically.</p>