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目的研究人巨细胞病毒(HCMV)感染对人神经胶质瘤U251细胞p38MAPK表达水平、细胞凋亡及细胞周期的影响。方法以免疫印迹法(WesternBlotting)分析HCMV感染人神经胶质瘤U251细胞后不同时间总p38MAPK、磷酸化p38MAPK蛋白表达水平;用流式细胞仪检测HCMV感染后人神经胶质瘤U251细胞凋亡百分率变化和细胞周期的分布。结果HCMV感染后不同时间U251细胞总p38蛋白的表达水平不变,但磷酸化p38于HCMV感染后6至10h明显增高,6h、10h平均灰度值分别为186.33±7.51和188.00±7.02,与对照组比较差异有统计学意义,16h后下降至基础水平。HCMV感染能诱导U251细胞凋亡,于感染后第5天凋亡率最高,达(10.18±1.24)%,与对照组比较差异有统计学意义。HCMV感染使G1期细胞明显减少,感染后2、5、7d分别减少至(56.50±2.57)%、(62.33±2.64)%和(67.45±4.44)%,与对照组比较差异均有统计学意义,细胞周期阻滞于S期和G2期。结论HCMV感染U251细胞能够激活p38MAPK,并诱导U251细胞凋亡、细胞周期阻滞。
Objective To study the effect of human cytomegalovirus (HCMV) infection on p38MAPK expression, apoptosis and cell cycle in human glioma U251 cells. Methods The total p38MAPK and phospho-p38MAPK protein expression in HCMV-infected human glioma U251 cells were detected by Western Blotting. The percentage of apoptotic cells in human glioma U251 cells was detected by flow cytometry Changes and cell cycle distribution. Results The expression level of total p38 protein in U251 cells was not changed at different time after HCMV infection. However, phosphorylation of p38 significantly increased from 6 to 10 hours after HCMV infection. The average gray values at 6h and 10h were 186.33 ± 7.51 and 188.00 ± 7.02, respectively, The difference between the two groups was statistically significant, down to the basic level after 16h. HCMV infection could induce apoptosis of U251 cells. The apoptosis rate of U251 cells was the highest (10.18 ± 1.24)% on the 5th day after infection, which was significantly different from the control group. HCMV infection significantly decreased the number of G1 phase cells and decreased to (56.50 ± 2.57)%, (62.33 ± 2.64)% and (67.45 ± 4.44)% on day 2, 5 and 7 after infection, respectively, , Cell cycle arrest in S phase and G2 phase. Conclusion HCMV infected U251 cells can activate p38MAPK and induce apoptosis and cell cycle arrest in U251 cells.