三氧化二砷体外对哮喘患者外周血T细胞凋亡和白细胞介素4分泌的影响(英文)

Effects of arsenic trioxide on apoptosis and interleukin-4 release of peripheral T cells from asthmatic patients in vitro

目的探讨三氧化二砷治疗哮喘的可能机制。方法分离21例哮喘患者和20例健康对照者外周血T细胞,分别加入三氧化二砷(0.1mg·L-1)或地塞米松(5mg·L-1)培养24 h。用ELISA方法检测培养上清液中白细胞介素4(IL-4)的含量,用荧光显微镜、流式细胞术和细胞色素c试剂盒检测细胞凋亡。结果哮喘患者T细胞自发释放IL-4较健康对照者明显增多;三氧化二砷对健康对照者T细胞IL-4的释放无影响,对哮喘患者T细胞IL-4释放增加具有抑制作用;地塞米松可使两组T细胞IL-4的释放明显降低。哮喘患者外周血T细胞体外培养24h凋亡百分率较健康对照者明显降低,细胞浆细胞色素c含量降低;三氧化二砷明显增加哮喘患者T细胞凋亡的百分率和细胞色素c的含量,对健康对照者作用不明显;地塞米松可使两组的T细胞凋亡百分率和细胞色素c含量增加。结论三氧化二砷治疗哮喘的机制可能与诱导哮喘患者T细胞凋亡和IL-4分泌减少有关。

AIM To study the possible mechanism of the treatment of arsenic trioxide on asthma. METHODS T cells isolated from 21 asthmatic patients and 20 healthy controls were treated with arsenic trioxide （0.1 mg· L^-1 ） or dexamethasone （5 mg· L^-1）, in vitro, for 24 h. Interleukin4 （IL4） levels in supernatants from T cells were quantified with ELISA. Cell apoptosis was measured by using fluorescence microscopy, flow cytometry and cytochrome c ELISA kit. RESULTS T cells of asthmatic patients spontaneously released more IL4 than that of healthy controls. Arsenic trioxide significantly decreased IL4 release of T cells from asthmatic patients, which was more obvious compared with healthy controls. Dexamethasone decreased IL4 release in both groups. Apoptosis percentage and cytochrome c content in cytoplasm of T cells from asthmatic patients were lower than those from healthy controls. Arsenic trioxide significantly increased the apoptosis percentage and cytochrome c content in cytoplasm of T cells in the asthmatic group, and had slighter effects on that in healthy controls. Dexamathasone increased the apoptosis percentage and cytochrome c content of T cells in both groups. CONCLUSION The mechanism of the treatment of arsenic trioxide on asthma involves the induction of T cell apoptosis and decrease of IL4 release in asthmatic patients.