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高继萍, 王裕, 杨霞, 皇甫冰, 陈朝阳, 郭民, 宋国华. 硒对氟诱导NRK-52E细胞凋亡干预作用机制[J]. 中国公共卫生, 2017, 33(1): 103-106. DOI: 10.11847/zgggws2017-33-01-26
引用本文: 高继萍, 王裕, 杨霞, 皇甫冰, 陈朝阳, 郭民, 宋国华. 硒对氟诱导NRK-52E细胞凋亡干预作用机制[J]. 中国公共卫生, 2017, 33(1): 103-106. DOI: 10.11847/zgggws2017-33-01-26
GAO Ji-ping, WANG Yu, YANG Xia.et al, . Mechanism of interference effect of selenium on sodium fluoride-induced apoptosis in NRK-52E cells[J]. Chinese Journal of Public Health, 2017, 33(1): 103-106. DOI: 10.11847/zgggws2017-33-01-26
Citation: GAO Ji-ping, WANG Yu, YANG Xia.et al, . Mechanism of interference effect of selenium on sodium fluoride-induced apoptosis in NRK-52E cells[J]. Chinese Journal of Public Health, 2017, 33(1): 103-106. DOI: 10.11847/zgggws2017-33-01-26

硒对氟诱导NRK-52E细胞凋亡干预作用机制

Mechanism of interference effect of selenium on sodium fluoride-induced apoptosis in NRK-52E cells

  • 摘要: 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 NaF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 NaF组比较,17.1、34.2 μg/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 NaF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 NaF组比较,17.1、34.2 g/L硒干预组AMPK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。

     

    Abstract: Objective To study antagonistic effect of selenium on sodium fluoride-induced apoptosis of NRK-52E cells.Methods NRK-52E cells were cultured and divided into following groups:a control group,two sodium fluoride (NaF)-treated (5,20 mg/L) groups,two sodium selenite (Na2SeO3)-treated (17.1,34.2 μg/L) groups,and four NaF+Na2SeO3-treated (5 or 20 mg/L NaF+17.1 or 34.2 μg/L Na2SeO3) groups.Cell apoptosis was detected by flow cytometry 72 hours after the treatments.Protein expressions of adenosine monophosphate-activated protein kinase (AMPK) and related mitochondria pathway proteins were determined using Western blot.Results Compared to the control group(5.97±0.09%),the cell apoptosis rate of the 5 and 20 mg/L NaF-treated groups (7.92±0.24% and 11.06±0.17%) were remarkably increased (P<0.05),while the rates of 20 mg/L NaF+17.1 and 34.2 g/L Na2SeO3-treated groups (8.46±0.09% and 9.88±0.08%) were statistically significantly decreased compared to that of the 20 mg/L NaF-treated groups (both P<0.05).Compared to those of the control group,the expression levels of phosphorylated-AMPK (0.73±0.16),bax (0.99±0.16),cytochrome C (Cyt-C)(0.73±0.08),caspase-9 (1.17±0.17),and caspase-3 (1.51±0.42) were obviously up-regulated in 20 mg/L NaF-treated group (P<0.05).Compared to those of the 20 mg/L NaF-treated group,the expression levels of phosphorylated -AMPK(046±0.12,0.48±0.15),bax(0.55±0.09,0.61±0.16),Cyt-C (0.30±0.06,0.34±0.05),caspase-9 (0.76±0.11,0.40±0.12),caspase-3 (0.35±0.1,0.27±0.04) were down-regulated in 20 mg/L NaF+17.1 and 34.2 g/L Na2SeO3-treated groups (all P<0.05).Conclusion Fluoride can induce apoptosis in NRK-52E cells and the effect can be ameliorated by selenium by regulation of AMPK mediated mitochondrial pathway.

     

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