CAJ | 학술논문

目的通过研究 188Re诱导前列腺癌 PC-3细胞、乳腺癌 ER-75-30细胞、肺癌 A549细胞凋亡的作用及相关基因 bcl-2和 bax在其中的表达,为临床个体化治疗及康复干预提供理论依据.方法人前列腺癌 PC-3细胞株、乳腺癌 ER-75-30细胞株和非小细胞肺癌 A549细胞株经培养后,采用光镜、电镜、流式细胞仪和免疫组化方法研究 188Re诱导 3种肿瘤细胞凋亡的形态学变化、时间剂量效应关系、细胞周期依赖性以及凋亡相关基因 bcl-2和 bax在其中的表达情况.结果 188Re能诱导肿瘤细胞产生凋亡的形态学变化,并且随着浓度的增大( 0～ 240 GBq/L)和时间的延长( 6～ 48 h),凋亡率增加, bcl-2表达减弱, bax表达增强,两者比值下降 (PC-3由 1.07± 0.56、 1.05± 0.48下降至 0.23± 0.10、 0.26± 0.10),细胞阻滞于 G2/M期. PC-3细胞对 188Re的敏感性最高,其次为 ER-75-30细胞, A549对 188Re的敏感性最低.结论 188Re电离辐射能诱导肿瘤细胞凋亡,且呈现时间剂量和周期依赖性; Bcl-2和 bax均参与 188Re诱导凋亡过程;不同肿瘤细胞对同一种核素的敏感性不同;并为临床个体化治疗和康复干预提供理论依据.
목적통과연구 188Re유도전렬선암 PC-3세포、유선암 ER-75-30세포、폐암 A549세포조망적작용급상관기인 bcl-2화 bax재기중적표체,위림상개체화치료급강복간예제공이론의거.방법인전렬선암 PC-3세포주、유선암 ER-75-30세포주화비소세포폐암 A549세포주경배양후,채용광경、전경、류식세포의화면역조화방법연구 188Re유도 3충종류세포조망적형태학변화、시간제량효응관계、세포주기의뢰성이급조망상관기인 bcl-2화 bax재기중적표체정황.결과 188Re능유도종류세포산생조망적형태학변화,병차수착농도적증대( 0～ 240 GBq/L)화시간적연장( 6～ 48 h),조망솔증가, bcl-2표체감약, bax표체증강,량자비치하강 (PC-3유 1.07± 0.56、 1.05± 0.48하강지 0.23± 0.10、 0.26± 0.10),세포조체우 G2/M기. PC-3세포대 188Re적민감성최고,기차위 ER-75-30세포, A549대 188Re적민감성최저.결론 188Re전리복사능유도종류세포조망,차정현시간제량화주기의뢰성; Bcl-2화 bax균삼여 188Re유도조망과정;불동종류세포대동일충핵소적민감성불동;병위림상개체화치료화강복간예제공이론의거.
Aim By studying apoptosis of human prostate cancer PC-3 cell, breast cancer ER-75-30 cell and lung cancer A549 cell induced by 188Re and detecting expression of bcl-2 and bax genes.We hope to offer theorical basis for clinical individual therapy and recovery interference.Methods Human prostate cancer PC-3 cell, breast cancer ER-75-30 cell and lung cancer A549 cell were cultured in RPMI medium 1640.Light microscope,transmissional electron microscope, flow cytometer and immunohistochemical method were used to observe apoptosis morphological changes of three kinds of tumor cell lines, time and dose effect relationship and to detect expression of bcl-2 and bax.Results 188Re can induce tumor cell producing apoptosis morphological changes.With the rise of radiative dose( 0- 240 GBq/L) and prolongation of culture time( 6- 48 h) , cell apoptosis induced by 188Re increased, expression of bcl-2 protein was enhanced and that of bax protein decreased. The ratio of bcl-2 and bax declined(declining from 1.07± 0.56,1.05± 0.48 to 0.23± 0.10,0.26± 0.10 in PC-3 cell line).Cells were blocked in G2/M period.PC-3 cell was most sensitive and A549 cell was most insensitive to 188Re.Conclusion 188Re can induce apoptosis of tumor cell, which have time and dose and cycle dependence.Both bcl-2 and bax genes play important roles in apoptosis.Diffrent cell line has diffrent sensitivity to 188Re.These can offer theorical basis for clinical individual therapy and recovery interference.