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目的 阿司匹林 (AS)对胃肠道肿瘤 ,特别是结肠癌有抑制作用 ,但对胃肠道外肿瘤是否也有作用并不清楚。探讨AS对H2 O2 诱导的SMMC772 1人肝癌细胞凋亡和坏死的作用及其机制。方法 应用细胞形态学、DNA片段电泳和流式细胞技术 ,测定乳酸脱氢酶 (LDH)释放率、细胞存活率及胞浆铁蛋白浓度 ,观察AS对H2 O2 所致的肝癌细胞凋亡和坏死的作用。结果 0 .8mmol/L的H2 O2 使肝癌细胞出现典型的亚二倍体Ap峰 ,“阶梯状”DNA电泳片段及凋亡细胞形态学改变 ;而 4mmol/L的H2 O2则引起细胞明显坏死 ;但临床剂量范围内 (≤ 5mmol/L)的AS不能诱导肝癌细胞凋亡 ,对H2 O2 所致的肝癌细胞凋亡和坏死有抑制作用。 0 .5mmol/LAS组可使Ap峰中细胞数 (凋亡率 )减少 34 % ,LDH释放率减少 40 % ,细胞存活率增加 50 % ;随着AS剂量加大 ,对凋亡和坏死的抑制作用也逐渐增强。5mmol/L的AS能完全对抗H2 O2 诱导的细胞凋亡 ,细胞坏死的情况也接近对照组 (P >0 .0 5) ;而去铁铁蛋白 (apo ferritin)也有类似的保护作用。检测发现AS能使肝癌细胞铁蛋白表达显著增加 ,与其抗凋亡及坏死作用有明显的相关性。结论 AS可保护SMMC772 1肝癌细胞对抗H2 O2 诱导的凋亡和坏死作用 ,其机制与AS增加肝癌细胞铁蛋白表达有关
Purpose Aspirin (AS) has an inhibitory effect on gastrointestinal tumors, especially colon cancer, but it is unclear whether it exerts any effect on parenteral tumors. To investigate the effect of AS on H 2 O 2 -induced apoptosis and necrosis in SMMC772 human hepatoma cells and its mechanism. Methods Lymphocyte dehydrogenase (LDH) release rate, cell viability and cytoplasmic ferritin concentration were determined by cell morphology, DNA fragment electrophoresis and flow cytometry. The effects of AS on H2O2-induced apoptosis and necrosis of hepatoma cells were observed Role. Results 0 .8mmol / L of H2O2 showed typical sub-diploid Ap peak, “ladder” DNA electrophoresis fragment and morphological changes of apoptotic cells, whereas 4mmol / L of H2O2 caused obvious cell necrosis. However, AS in the range of clinical dose (≤ 5 mmol / L) failed to induce apoptosis of hepatocellular carcinoma cells and inhibited the apoptosis and necrosis of hepatoma cells induced by H2O2. At 0. 5mmol / LAS, the number of apoptotic cells in Ap peak decreased by 34%, the release rate of LDH decreased by 40%, and the cell survival rate increased by 50%. With the increase of AS dose, the inhibition of apoptosis and necrosis The role is also gradually enhanced. 5 mmol / L AS completely antagonized the H2O2-induced apoptosis, the cell necrosis was also close to the control group (P> 0.05); and apo ferritin also have similar protective effect. It was found that AS can significantly increase the expression of ferritin in hepatocellular carcinoma cells, and has obvious correlation with its anti-apoptotic and necrotic effects. Conclusion AS can protect SMMC772 hepatoma cells against H2O2-induced apoptosis and necrosis, and its mechanism is related to the increased expression of ferritin in hepatoma cells by AS