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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。
Objective To investigate the possible mechanism of arsenic trioxide in the treatment of asthma. Methods Peripheral T cells from 21 asthmatic patients and 20 healthy controls were isolated and cultured for 24 h with arsenic trioxide (0.1 mg · L -1) or dexamethasone (5 mg · L -1) respectively. The content of interleukin-4 (IL-4) in culture supernatant was detected by ELISA. Apoptosis was detected by fluorescence microscopy, flow cytometry and cytochrome c kit. Results The spontaneous release of IL-4 from T cells in asthmatic patients was significantly increased compared with that in healthy controls. Arsenic trioxide had no effect on the release of IL-4 from T cells in healthy controls and IL-4 release from T cells in asthmatic patients. Dexamethasone The release of IL-4 from both T cells was significantly reduced. The percentage of apoptotic T lymphocytes in peripheral blood of asthmatic patients was significantly lower than that of healthy controls at 24 h, and the content of cytochrome c was decreased. Arsenic trioxide significantly increased the percentage of apoptotic T cells and cytochrome c in asthmatic patients, Not obvious; dexamethasone can make both the percentage of T cell apoptosis and cytochrome c increased. Conclusion The mechanism of arsenic trioxide in treating asthma may be related to the decrease of T cell apoptosis and IL-4 secretion induced by asthma.