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目的探讨艰难梭菌毒素A(TcdA)对白血病细胞株K562增殖、凋亡的作用及其机制。方法采用四唑蓝比色试验(MTT)检测TcdA对K562细胞增殖的影响;流式细胞术(FCM)检测细胞凋亡情况;RT-PCR法检测TcdA作用后细胞Bcl-2/Bax,Egr-1mRNA表达的变化。结果 TcdA能抑制K562细胞的增殖,作用48h后的抑制率(IR)为47.67%,流式细胞仪分析出现典型的亚二倍体峰(凋亡峰)。TcdA作用后K562细胞Bcl-2基因表达下调,Bax基因表达上调,而Egr-1基因表达上调,并呈量效关系。结论艰难梭菌毒素A可诱导K562细胞凋亡,其机制可能与下调Bcl-2,上调Bax,上调Egr-1基因表达水平有关。
Objective To investigate the effect and mechanism of Clostridium difficile toxin A (TcdA) on proliferation and apoptosis of leukemia cell line K562. Methods The effect of TcdA on the proliferation of K562 cells was detected by tetrazolium blue colorimetric assay (MTT); apoptosis was detected by flow cytometry (FCM); Bcl-2/Bax and Egr- were detected by RT-PCR after TcdA treatment. 1 Changes in mRNA expression. Results The proliferation of K562 cells was inhibited by TcdA. The inhibition rate (IR) after 48 h was 47.67%. Typical subdiploid peaks (apoptotic peaks) were detected by flow cytometry. After TcdA treatment, the expression of Bcl-2 gene was down-regulated in K562 cells, and the expression of Bax gene was up-regulated, but the expression of Egr-1 gene was up-regulated, showing a dose-effect relationship. Conclusion C. difficile toxin A can induce apoptosis in K562 cells, which may be related to the down-regulation of Bcl-2, up-regulation of Bax, and up-regulation of Egr-1 gene expression.