过表达Apg-2对H2O2诱导的BaF3-BCR/ABL细胞损伤的保护作用

目的 观察过表达Apg-2对H2O2所致BaF3-BCR/ABL细胞损伤的保护作用。 方法 以H2O2作用于逆转录病毒空载体MIGR1感染细胞株BaF3-MIGR1和稳定表达BCR/ABL的BaF3-BCR/ABL细胞为氧化应激损伤模型，RT-PCR检测H2O2作用前后Apg-2基因表达水平；用紫外分光光度法测定乳酸脱氢酶(LDH)释放率，观察细胞的损伤程度；硫代巴比妥酸法测定丙二醛(MDA)含量，黄嘌呤氧化酶法测定过氧化物歧化酶(SOD)活性；Am-blue法检测细胞存活率。 结果 过表达Apg-2能明显改善H2O2导致的BaF3-BCR/ABL细胞损伤，与BaF3-MIGR1细胞处理组相比，过表达Apg-2可使BaF3-BCR/ABL细胞存活率升高，LDH释放率明显降低，降低MDA含量，提高SOD活性。 结论 过表达Apg-2对H2O2诱导的BaF3-BCR/ABL细胞损伤具有明显的保护作用。

Protective effect of Apg-2 overexpression on BaF3-BCR/ABL cell injury induced by hydrogen dioxide

Objective To observe the protective effect of Apg-2 overexpreesion on BaF3-BCR/ABL cell injury induced by hydrogen dioxide (H2O2). Methods The models of oxidative stress damage of BaF3 MIGR1 and BaF3-BCR/ABL cell infected with retrovirus vector MIGR1 were induced by hydrogen dioxide. The expression level of Apg-2 which exposed to hydrogen dioxide was detected by RT-PCR. The release of lactate dehydrogenase (LDH) was detected by ultraviolet spectrophometry to evaluate the degree of injury. The content of malondialdehyde (MDA) was measured by thiobarbituric acid and peroxide dismutase (SOD) activity was measured by xanthine oxidese method. The cell viability was tested by Am Blue assay. Results Apg-2 overexpression significantly reduced BaF3-BCR/ABL cell injury induced by hydrogen dioxide. Compared with the cells treated with BaF3-MIGR1, Apg-2 overexpression in BaF3-BCR/ABL cell improved cellular viability, reduced LDH release and MDA content, increase of SOD activity. Conclusion Apg 2 overexpression exhibited significant protective effect on BaF3-BCR/ABL cell injury induced by hydrogen dioxide.