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目的:研究GRP-78和caspase-12在氟致大鼠成釉细胞内质网应激和细胞凋亡中的作用,探讨氟所介导的内质网应激是否导致细胞凋亡。方法:应用CCK8和流式细胞术观察不同浓度的氟对成釉细胞活性及凋亡数量的影响,以实时定量PCR和Western印迹法检测氟对内质网伴侣分子GRP-78和caspase-12基因和蛋白表达的影响,应用SPSS13.0软件包对数据进行统计学分析。结果:随着氟浓度的不断增加,大鼠成釉细胞活性呈逐渐下降趋势,流式细胞术同样显示发生凋亡的细胞数量逐渐上升;实时定量RT-PCR和Western印迹结果显示,GRP-78和caspase-12的表达量随着氟浓度增加而增加。结论:过量氟介导了大鼠成釉细胞内质网应激,并且通过内质网应激,引起细胞凋亡。
OBJECTIVE: To investigate the role of GRP-78 and caspase-12 in the regulation of endoplasmic reticulum stress and apoptosis induced by fluoride in rat ameloblasts, and to explore whether fluoride-mediated endoplasmic reticulum stress leads to apoptosis. Methods: CCK8 and flow cytometry were used to observe the effect of different concentrations of fluoride on the activity of ameloblasts and the number of apoptotic cells. Real-time PCR and Western blotting were used to detect the expression of GRP-78 and caspase-12 And protein expression, using SPSS13.0 software package for statistical analysis of the data. Results: With the continuous increase of fluoride concentration, the ameloblasts activity of rats decreased gradually. Flow cytometry also showed that the number of apoptotic cells increased gradually. Real-time quantitative RT-PCR and Western blotting showed that GRP-78 And caspase-12 expression increased with increasing fluoride concentration. CONCLUSION: Excessive fluoride mediates endoplasmic reticulum stress in rat ameloblasts and induces apoptosis through endoplasmic reticulum stress.