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目的探讨 L-精氨酸诱导人肝癌细胞凋亡的作用及机制。方法采用倒置显微镜、透射电镜和流式细胞仪,观察和分析不同浓度 L-精氨酸作用下体外培养人肝癌细胞株 QGY-7703的增殖和凋亡情况。结果 (1)低浓度 L-精氨酸对肝癌细胞生长和细胞大体形态无明显影响。高浓度的L-精氨酸引起肝癌细胞形态变圆、体积变小,细胞皱缩,细胞核固缩,核碎裂,染色质边聚,凋亡小体形成。(2)低浓度 L-精氨酸对肝癌细胞生长周期和增殖指数无影响;而高浓度的 L-精氨酸引起 G_0/G_1期较对照组显著升高,S 期显著降低,细胞增殖指数显著下降(P<0.05),而 G_2/M 无明显变化。(3)低浓度 L-精氨酸(1mmol/L)和对照组细胞未见凋亡峰(亚 G_1峰),凋亡率分别为2.1%和2.5%;而16mmol/L和64mmol/L 浓度组则出现典型的凋亡峰,凋亡率分别为12.4%和30.8%,较对照组显著增高(P<0.05)。结论高浓度的 L-精氨酸通过合成 NO,诱导肝癌细胞凋亡。
Objective To investigate the effect and mechanism of L-arginine-induced apoptosis in human hepatoma cells. Methods The proliferation and apoptosis of human hepatoma cell line QGY-7703 cultured in vitro were observed and analyzed by inverted microscope, transmission electron microscope and flow cytometry. Results (1) Low concentration of L-arginine had no significant effect on the growth of hepatoma cells and the general morphology of hepatoma cells. High concentrations of L-arginine cause liver cancer cells become round, smaller, cell shrinkage, nuclear pyknosis, nuclear fragmentation, chromatin edge aggregation, apoptotic body formation. (2) Low concentration of L-arginine had no effect on the growth and proliferation index of hepatocellular carcinoma cells. However, the high concentration of L-arginine induced a significant increase in G_0 / G_1 phase compared with the control group, S phase decreased significantly, the cell proliferation index (P <0.05), while G 2 / M did not change significantly. (3) No apoptotic peak (sub-G_1 peak) was detected in low concentration of L-arginine (1mmol / L) and control group, the apoptotic rate was 2.1% and 2.5% respectively; while 16mmol / L and 64mmol / L The typical apoptotic peak appeared in the group with a apoptotic rate of 12.4% and 30.8% respectively, which was significantly higher than that of the control group (P <0.05). Conclusion L-arginine at high concentration induces apoptosis of hepatoma cells through NO synthesis.