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目的探讨碘过量对人正常甲状腺细胞(Nthy-ori 3-1)的损伤作用及机制。方法用0(对照)、1、10、50mmol/L的碘化钾(KI)作用于体外培养的Nthy-ori 3-1细胞24 h后,分别采用噻唑蓝(MTT)法、乳酸脱氢酶(LDH)比色法检测细胞存活率和LDH漏出率,利用流式细胞术检测活性氧(ROS)水平、细胞周期构成比及凋亡率。结果与对照组相比,50 mmol/L碘染毒组细胞存活率明显下降(P<0.05),LDH漏出率明显上升(P<0.05)。各剂量组之间ROS产生水平差异无统计学意义。50 mmol/L碘染毒组G0/G1期细胞百分比明显增多(P<0.05),但S期百分比明显减少(P<0.05),且细胞凋亡率明显上升(P<0.05)。结论一定剂量的碘能降低甲状腺细胞存活率,增加LDH漏出率,细胞G0/G1期阻滞和诱导细胞凋亡,碘对甲状腺的损伤作用可能与碘对细胞周期的影响有关。
Objective To investigate the effect of iodine excess on the damage of normal thyroid cells (Nthy-ori 3-1) and its mechanism. Methods Nthy-ori 3-1 cells cultured in vitro were treated with 0 (control), 1,10,50 mmol / L potassium iodide (KI) for 24 h, then treated with MTT method and lactate dehydrogenase ) Cell viability and LDH leakage rate were detected by colorimetric assay. The levels of reactive oxygen species (ROS), cell cycle components and apoptotic rate were determined by flow cytometry. Results Compared with the control group, the cell viability in 50 mmol / L iodine treatment group decreased significantly (P <0.05), and the LDH leakage rate increased significantly (P <0.05). There was no significant difference in the level of ROS production between each dose group. The percentage of cells in G0 / G1 phase of 50 mmol / L iodine treatment group was significantly increased (P <0.05), but the percentage of S phase was significantly decreased (P <0.05), and the apoptosis rate was significantly increased (P <0.05). Conclusion A certain dose of iodine can reduce thyroid cell viability, increase LDH leakage rate, block G0 / G1 arrest and induce cell apoptosis. The effect of iodine on thyroid damage may be related to the effect of iodine on cell cycle.