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目的探讨丙酮醛对人肾近端小管上皮细胞(HK-2细胞)损伤的作用及可能机制。方法采用不同浓度的丙酮醛(100、200、400、800、1 600μmol/L)处理HK-2细胞24 h后,应用CCK-8法检测HK-2细胞的存活率;罗丹明123染色法检测细胞线粒体膜电位;DAPI染色法观察HK-2细胞凋亡形态学变化。Western blot法检测HK-2细胞内磷酸化ERK1/2(phosphated ERK1/2,p-ERK1/2)、Bax及cleaved-caspase-3蛋白表达水平。结果与对照组相比,不同的浓度的丙酮醛均能降低HK-2细胞存活率(P<0.01);且HK-2细胞经丙酮醛诱导后cleaved-caspase-3(P<0.01)、Bax及p-ERK1/2蛋白表达水平均明显增高(P<0.05)。结论丙酮醛能诱导HK-2细胞出现明显的损伤及凋亡,其机制可能与其激活ERK1/2信号通路有关。
Objective To investigate the effect and possible mechanism of pyruvate on the injury of human renal proximal tubular epithelial cells (HK-2 cells). Methods HK-2 cells were treated with different concentrations of pyruvate (100, 200, 400, 800 and 600 μmol / L) for 24 h. The viability of HK-2 cells was detected by CCK- Cell mitochondrial membrane potential and DAPI staining were used to observe the morphological changes of HK-2 cells. The protein expression of phosphorylated ERK1 / 2, p-ERK1 / 2, Bax and cleaved-caspase-3 in HK-2 cells was detected by Western blot. Results Compared with the control group, different concentrations of pyruvate decreased the viability of HK-2 cells (P <0.01), and the expression of cleaved-caspase-3 (P <0.01), Bax And p-ERK1 / 2 protein expression were significantly increased (P <0.05). Conclusion Pyruvate can induce obvious injury and apoptosis in HK-2 cells, which may be related to its activation of ERK1 / 2 signaling pathway.