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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 study the inhibitory effect of adenovirus-mediated IL-24 gene expression vector (Ad-IL-24) on human glioma U87MG cells and to explore its possible mechanism. Methods: The U87MG cells were infected with Ad-IL-24 and the expression of IL-24 was detected by RT-PCR. The growth and apoptosis of U87MG cells were detected by MTT assay and flow cytometry. The expression of U87MG The morphological changes of apoptosis were observed. The mRNA expressions of Bax and Bcl-2 were detected by RT-PCR. The activation of caspase-3 was detected by Western blotting. Results: After U87MG cells were infected with Ad-IL-24, IL-24 was significantly expressed in U87MG cells and inhibited the growth of U87MG cells. The apoptosis of U87MG cells induced by Ad-IL-24 showed a typical apoptotic nuclear morphological changes. Ad-IL-24 up-regulated the Bax gene in U87MG cells, down-regulated the expression of Bcl-2 gene and induced the activation of caspase-3 protein. Conclusion: Ad-IL-24 can induce the apoptosis of U87MG cells. The mechanism may be related to the up-regulation of Bax gene, down-regulation of Bcl-2 gene expression and activation of caspase-3.