目的：研究腺病毒介导IL-24基因表达载体(Ad-IL-24)对人脑胶质瘤U87MG细胞的抑制作用，初步探讨其作用机制。方法：将本科室构建的Ad-IL-24感染U87MG细胞，RT-PCR法检测IL-24基因的表达，MTT法和流式细胞术检测U87MG细胞的生长和凋亡，激光共聚焦显微镜观察U87MG细胞凋亡的形态学变化，RT-PCR法检测Bax、Bcl-2基因mRNA的表达，Western blotting检测caspase-3的活化。结果：Ad-IL-24感染U87MG细胞后，IL-24在U87MG细胞中有明显表达，并抑制U87MG细胞生长、诱导其凋亡、出现典型的凋亡细胞核形态学改变。Ad-IL-24可上调U87MG细胞中Bax基因、下调Bcl-2基因的表达，并诱导caspase-3蛋白的活化。结论：Ad-IL-24可诱导U87MG细胞凋亡，其机制可能与上调Bax基因、下调Bcl-2基因表达，并活化caspase-3有关。

Objective: To investigate the inhibitory effect of adenovirus-mediated IL-24 (Ad-IL-24) on human glioma U87MG cells and to explore the underlying molecule mechanism. Methods: U87MG cells were infected with Ad-IL-24 constructed in our department, and IL-24 gene expression in U87MG cells was detected by RT-PCR. The growth and apoptosis of U87MG cells were examined by MTT and flow cytometry; the morphological change of U87MG cells was observed by laser scanning confocal microscopy; the Bax and Bcl-2 mRNA expressions were analyzed by RT-PCR; and the activation of caspase-3 was examined by Western blotting analysis. Results: The IL-24 gene was expressed in Ad-IL-24-infected U87MG cells. Ad-IL-24-infection inhibited the growth and induced apoptosis of U87MG cells, which showed typical morphological changes of apoptotic nuclei. Moreover, Ad-IL-24 increased Bax and decreased Bcl-2 mRNA expression, and induced caspase-3 activation in U87MG cells. Conclusion: Ad-IL-24 can induce apoptosis of U87MG cells, probably through up-regulating Bax expression, down-regulating Bcl-2 expression, and inducing caspase-3 activation.

江苏省高校自然科学基础研究项目(No. 08KJB310011)