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目的探讨信号转导和转录激活因子-5(STAT5)的表达在不同程度慢性苯中毒诱导细胞凋亡中的作用及其发生机制。方法以53例慢性苯中毒患者(轻度苯中毒组28例、中度苯中毒组12例、重度苯中毒组13例)和20例正常对照者为研究对象,应用半定量反转录聚合酶链式反应(RT-PCR)法检测骨髓单个核细胞(STAT5)的信使核糖核酸(mRNA)表达,应用流式细胞仪(FCM)检测骨髓造血细胞细胞凋亡率的变化。结果 STAT亚型5A(STAT5A)未参与苯中毒诱导的凋亡。中、重度苯中毒组STAT亚型5B(STAT5B)表达均低于正常对照组和轻度苯中毒组,差异均有统计学意义(P<0.05);重度苯中毒组STAT5B表达低于中度苯中毒组,差异有统计学意义(P<0.05);中、重度苯中毒组细胞凋亡率高于正常对照组和轻度苯中毒组,差异有统计学意义(均P<0.05);重度苯中毒组细胞凋亡率高于中度苯中毒组,差异有统计学意义(P<0.05)。结论慢性中、重度苯中毒患者STAT5B mRNA的表达降低,STAT5信号转导通路异常在苯诱导细胞凋亡增加发病机制中起重要作用。
Objective To investigate the role of STAT5 in apoptosis induced by chronic benzene poisoning and its mechanism. Methods 53 patients with chronic benzene poisoning (mild benzene poisoning group of 28 cases, moderate benzene poisoning group of 12 cases, severe benzene poisoning group of 13 cases) and 20 cases of normal control subjects were studied by semi-quantitative reverse transcriptase polymerase The expression of messenger RNA (mRNA) in bone marrow mononuclear cells (STAT5) was detected by reverse transcription polymerase chain reaction (RT-PCR). The apoptosis rate of bone marrow hematopoietic cells was detected by flow cytometry (FCM). Results STAT subtype 5A (STAT5A) did not participate in benzene poisoning induced apoptosis. The expression of STAT5B in moderate and severe benzene poisoning group was lower than that in normal control group and mild benzene poisoning group (P <0.05), and the expression of STAT5B in severe benzene poisoning group was lower than that of moderate benzene (P <0.05). The rate of apoptosis in moderate and severe benzene poisoning group was higher than that in normal control group and mild benzene poisoning group (all P <0.05). Heavy benzene The apoptosis rate of poisoning group was higher than that of moderate benzene poisoning group, the difference was statistically significant (P <0.05). Conclusion The expression of STAT5B mRNA is decreased in patients with chronic moderate or severe benzene poisoning. The abnormal STAT5 signal transduction pathway plays an important role in the pathogenesis of benzene-induced apoptosis.