γ辐射诱发的人AHH-1 T淋巴细胞凋亡及其调控机制

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

目的 :研究电离辐射诱发正常人AHH 1T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 1T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 1T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cas pase

AIM: To explore the apoptotic characteristics and modulatory mechanism of human AHH-1 T lymphoblaste 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. ③The 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.