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本研究观察了三氧化二砷对哮喘患者T细胞凋亡、白细胞介素-4分泌的影响,并探讨了Bc l-2的作用。分离哮喘患者(n=21)和健康对照者(n=20)的外周血T细胞,分别加入三氧化二砷和地塞米松培养24 h。用荧光显微术、流式细胞仪DNA含量分析法和细胞色素c ELISA试剂盒检测T细胞凋亡,用ELISA的方法测量血清和细胞培养上清液白细胞介素-4水平,用免疫荧光流式细胞分析法测定Bc l-2基因表达。与健康对照者比较,哮喘患者T细胞体外培养24 h后自发凋亡减慢。地塞米松使哮喘患者和健康对照者的T细胞凋亡率均增加,两试验组间增加幅度无显著差异。三氧化二砷显著增加哮喘患者T细胞凋亡率,但对健康对照者T细胞凋亡影响不明显。哮喘患者血清白细胞介素-4水平升高,T细胞Bcl-2表达上调。而且,在体外培养24 h后,哮喘患者T细胞比健康对照者T细胞自发分泌的白细胞介素-4及Bcl-2的表达水平均有所提高。三氧化二砷显著减少哮喘患者T细胞白细胞介素-4分泌,下调Bcl-2表达,但对健康对照者T细胞无明显影响。地塞米松可使两试验组T细胞释放白细胞介素-4显著减少,但对两试验组T细胞Bcl-2基因表达影响不明显。结果提示:三氧化二砷在体外可诱导哮喘患者T细胞凋亡,减少白细胞介素-4分泌,下调Bcl-2基因表达可能是其重要机制之一。
This study examined the effects of arsenic trioxide on T cell apoptosis and interleukin-4 secretion in asthmatic patients and explored the role of Bcl-2. Peripheral blood T cells from asthmatic patients (n = 21) and healthy controls (n = 20) were isolated and cultured with arsenic trioxide and dexamethasone for 24 h. Fluorescence microscopy, flow cytometry DNA content analysis and cytochrome c ELISA kit detection of T cell apoptosis, serum and cell culture supernatants were measured by ELISA ELISA interleukin -4 levels by immunofluorescence flow Bc 1-2 gene expression was determined by the cell-based assay. Compared with healthy controls, spontaneous apoptosis of T-cells from asthmatic patients slowed down after cultured for 24 h in vitro. Dexamethasone asthma patients and healthy controls were T-cell apoptosis rates were increased, no significant difference between the two test groups. Arsenic trioxide significantly increased the apoptotic rate of T cells in asthmatic patients, but had no obvious effect on T cell apoptosis in healthy controls. Serum interleukin-4 levels in asthmatic patients were elevated, and Bcl-2 expression was up-regulated in T cells. Moreover, the levels of interleukin-4 and Bcl-2 secreted by T cells from asthmatic patients were significantly higher than those from healthy controls 24 hours after in vitro culture. Arsenic trioxide significantly reduced interleukin-4 secretion and down-regulated the expression of Bcl-2 in asthmatic patients, but had no significant effect on T cells in healthy controls. Dexamethasone significantly decreased the release of interleukin-4 from T cells in both experimental groups, but had no obvious effect on the expression of Bcl-2 gene in T cells in both experimental groups. The results suggest that arsenic trioxide can induce the apoptosis of T cells in asthmatic patients, reduce the secretion of interleukin-4 and down-regulate the expression of Bcl-2 gene in vitro, which may be one of the important mechanisms.