γ辐射诱发的人AHH-1 T淋巴细胞凋亡及其调控机制

目的：研究电离辐射诱发正常人AHH-1 T淋巴母细胞凋亡的特点及其调控机制，为辐射免疫损伤的防治提供实验依据。方法：用TUNEL、麦格-姬姆萨(MGG)法、MTT比色法及碱磷酶免疫组织化学染色法。分别检测T细胞凋亡、细胞活存以及Bax、Bcl-XL和caspase-3重要凋亡相关蛋白的表达及规律。结果：①在一定照射剂量范围内随照射剂量的增加，AHH-1 T细胞凋亡率持续升高，而细胞活的活存率则急剧下降，两者均呈现明显的剂量效应关系。②促凋亡蛋白Bax的表达随照射剂量的增加明显增强，而凋亡抑制蛋白Bcl-XL则呈持续下降的趋势。③活化的凋亡执行蛋白caspase-3的活性随照射剂量的增加显著升高，与凋亡率呈现明显的相应关系。结论：AHH-1 T细胞的大量凋亡，可能是辐射导致淋巴细胞急剧减少、机体免疫功能降低的重要原因；Bax、Bcl-XL和caspase-3蛋白在辐射诱发的T细胞凋亡调控中具有重要作用。

Apoptosis and modulatory mechanism of human AHH-1 T lymphocytes induced by γ-irradiation

AIM: To explore the apoptotic characteristics and modulatory mechanism of human AHH-1 T lymphoblast induced by ionizing radiation and provide an experimental basis for preventing and treating immune damage in acute radiation sickness. METHODS: TdT-mediated dUTP nick end labeling (TUNEL) and May-Grunwald Giemsa (MGG) staining, MTT colorimetry and immunohistochemical staining were used to detect the T lymphocyte apoptosis, cell survival and the expressions of Bax, Bcl-XL and caspase-3 proteins. RESULTS: (1) Over a definite dose range, apoptotic rate of AHH-1T lymphocytes increased with the elevation of radiation doses, while the lymphocytic survival rate decreased sharply, both showing a good dose-effect relationship. (2) The expression of apoptosis-accelerating protein Bax enhanced obviously with the increase of radiation doses, while apoptosis-inhibiting protein Bcl-XL trended to persistent decline. (3)The activity of activated apoptosis-executing protein caspase-3 heightened significantly with increased radiation doses, which revealed a better corresponding relationship to apoptotic rate. CONCLUSION: A great number of apoptotic AHH-1 T cells may be one of major accounts for the lymphocyte rapid reduction and depressed organism immune function induced by irradiation. Bax, Bcl-XL and caspase-3 proteins play an important role in the regulation of radiation-induced T cell apoptosis.