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目的探讨硒对氟诱导NRK-52E细胞凋亡的拮抗作用。方法实验设对照组、染氟组、染硒组、硒干预组,培养NRK-52E细胞,染毒72 h,采用流式细胞仪检测细胞凋亡,Western blot检测AMPK及线粒体通路相关蛋白表达水平。结果与对照组[(5.97±0.09)%]比较,5、20 mg/L Na F组细胞凋亡率[分别为(7.92±0.24)%、(11.06±0.17)%]明显升高(P<0.05);与20 mg/L Na F组比较,17.1、34.2μg/L硒干预组细胞凋亡率[分别为(8.46±0.09)%、(9.88±0.08)%]明显降低(P<0.05);与对照组比较,20 mg/L Na F组细胞AMPK磷酸化蛋白、bax、Cyt-C蛋白表达[分别为(0.73±0.16)、(0.99±0.16)、(0.73±0.08)]、活性caspase-9和caspase-3蛋白表达[分别为(1.17±0.17)、(1.51±0.42)]均升高(P<0.05);与20 mg/L Na F组比较,17.1、34.2 g/L硒干预组AM PK磷酸化蛋白表达量[分别为(0.46±0.12)、(0.48±0.15)]、bax、Cyt-C蛋白表达量[分别为(0.55±0.09)、(0.61±0.16)与(0.30±0.06)、(0.34±0.05)]及活性caspase-9、caspase-3蛋白表达量[分别为(0.76±0.11)、(0.40±0.12)与(0.35±0.12)、(0.27±0.04)]均降低(P<0.05)。结论 AMPK介导的线粒体通路参与了硒拮抗氟诱导NRK-52E细胞凋亡过程。
Objective To investigate the antagonistic effect of selenium on fluorine-induced apoptosis in NRK-52E cells. Methods The NRK-52E cells were cultured in the control group, the fluoride-exposed group, the selenium-contaminated group and the selenium-treated group. The cells were cultured for 72 h. The apoptosis of cells was detected by flow cytometry. The expression of AMPK and mitochondrial pathway- . Results Compared with the control group [(5.97 ± 0.09)%], the apoptotic rate of 5,20 mg / L NaF group was significantly higher than that of the control group [(7.92 ± 0.24)% and (11.06 ± 0.17)%, respectively] 0.05). Compared with the 20 mg / L NaF group, the apoptotic rate of the cells treated with 17.1,34.2μg / L selenium [(8.46 ± 0.09)%, (9.88 ± 0.08)%] were significantly decreased (P <0.05) ; Compared with the control group, the expression of AMPK phosphorylation protein, bax and Cyt-C in 20 mg / L NaF group were significantly higher than that in the control group [(0.73 ± 0.16), (0.99 ± 0.16), (0.73 ± 0.08) (1.17 ± 0.17) and (1.51 ± 0.42), respectively (P <0.05). Compared with 20 mg / L NaF group, selenium intervention with 17.1 and 34.2 g / L (0.46 ± 0.12) and (0.48 ± 0.15), respectively. The protein expression of bax and Cyt-C were (0.55 ± 0.09), (0.61 ± 0.16) and (0.30 ± (0.36 ± 0.11), (0.40 ± 0.12) and (0.35 ± 0.12), (0.27 ± 0.04)] were significantly lower than those in the control group (P <0.01), and the expression of caspase-3 and caspase- (P <0.05). Conclusion AMPK-mediated mitochondrial pathway is involved in the selenium antagonism of fluoride-induced apoptosis in NRK-52E cells.