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目的研究注射用核糖核酸Ⅱ诱导人白血病细胞系K562和KG1a细胞凋亡的作用。方法以K562和KG1a细胞为研究对象,采用CCK-8法检测注射用核糖核酸Ⅱ对细胞增殖的影响;流式细胞术检测细胞凋亡率的变化;Hoechst33258染色观察细胞核形态;免疫印迹技术检测p53及凋亡相关蛋白Bcl-2、Bax和cleaved caspase-3的表达。结果以100~300 mg·L~(-1)注射用核糖核酸Ⅱ处理K562和KG1a细胞12、24、48 h后,CCK-8检测结果显示K562和KG1a细胞的增殖降低,抑制率明显增高,并呈时间剂量依赖性;100、150、200mg·L~(-1)注射用核糖核酸Ⅱ处理K562和KG1a细胞24 h后,FCM结果显示细胞凋亡率随药物剂量增加而增高;Hoechst33258染色观察到细胞核出现染色质浓缩聚集、染色加深等凋亡指征;Western blot结果显示,注射用核糖核酸Ⅱ上调p53、Bax和cleaved caspase-3的表达,下调Bcl-2表达。结论注射用核糖核酸Ⅱ通过上调p53,调控Bcl-2/Bax的表达,激活caspase-3诱导人白血病K562和KG1a细胞凋亡。
Objective To study the effect of RNA Ⅱ for injection on the apoptosis of human leukemia cell lines K562 and KG1a. Methods K562 and KG1a cells were used as the research objects. The effects of ribonucleic acid Ⅱ for injection on cell proliferation were detected by CCK-8 assay. The changes of cell apoptosis were detected by flow cytometry. The morphology of nucleus was observed by Hoechst33258 staining. And the expression of apoptosis-related proteins Bcl-2, Bax and cleaved caspase-3. Results After K562 and KG1a cells were treated with 100-300 mg · L -1 ribonucleic acid for 12,24 and 48 h, the proliferation of K562 and KG1a cells was decreased and the inhibition rate was significantly increased. And in a time-dose-dependent manner; FCM results showed that the apoptosis rate of K562 and KG1a cells treated with 100,150,200 mg · L -1 RNAi Ⅱ increased with the increase of the dose of HNR31; 24 h after Hoechst33258 staining, The results showed that RNA Ⅱ could up-regulate the expression of p53, Bax and cleaved caspase-3, and down-regulate Bcl-2 expression. Conclusion Ribonucleic acid Ⅱ for injection induces caspase-3-induced apoptosis in human leukemia K562 and KG1a cells by up-regulating p53, regulating Bcl-2 / Bax expression.