镉诱导LLC-PK_1细胞凋亡对基因表达的影响

Effect of cadmium on apoptosis and expression of bcl-2,p53,c-myc,c-fos and ras genes in LLC-PK_1 cells

目的探讨镉诱导猪肾近曲小管上皮细胞(LLC-PK1)凋亡对bcl-2、p53(mtp53)、c-mycc、-fos与ras基因表达的影响。方法采用流式细胞仪分别测定bcl-2、p53、c-myc、c-fos与ras基因表达产物。结果不同浓度CdCl2(0,10,20,40μmol/L)作用LLC-PK1细胞,8 h后bcl-2表达逐渐下降,并呈良好的剂量-反应关系(r=-0.910,P<0.05);4,8 h p53表达均明显下降,呈剂量-反应关系(r值分别为-0.716,-0.972,P均<0.05);8 h后c-myc表达逐渐下降,呈剂量-反应关系(r=-0.694,P<0.05);8 h后c-fos表达未见剂量-反应关系;8 h后ras表达逐渐下降,呈明显的剂量-反应关系(r=-0.887,P<0.05)。结论镉诱导LLC-PK1细胞凋亡的机制可能与镉抑制bcl-2、p53、c-mycr、as基因表达有关。

Objective To explore the effect of cadmium on the apoptesis of porcine renal proximal tubtde epithelial cells（LLC-PK1 ）and the relationship between the apoptosis and the bcl-2, p53, c-myc, c-los and ras gene expression. Methods The expression of bcl-2, p53, c-myc, c-los and ras were measured respectively by FCM. Results After LLC-PK1 cells were incubated with 0,10, 20, 40 μmol/L CdCl2 for 4 h or 8 h, the expression of bcl-2, p53, c-myc and ras decreased and there was a significant dose-response relationship（ r=-0.910 of bcl-2 for 8 h, r=- 0.716,-0.972 of p53 for 4 h, 8 h respectively, r=-0. 694 of c-myc for 8 h and r =-0.887 of ras for 8 h）. Conclusion The apoptesis of LLC-PK1 cells could be induced by cadmium, and the inhibition of the expression of bcl-2, p53, c-myc and ras wotdd be one possible mechanism.