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目的观察IRE1通路在高碘诱导甲状腺细胞凋亡中的特征,进一步分析高碘诱导甲状腺细胞凋亡的作用机制。方法用0(对照)、1、10、50 mmol/L的碘化钾(KI)染毒体外培养的Nthy-ori 3-1细胞,24 h后采用流式细胞术检测Nthy-ori 3-1细胞凋亡率,用荧光定量PCR及Western blot检测葡萄糖调节蛋白78(GRP78)、肌醇需求酶-1(IRE1)、CCAAT/增强子结合蛋白同源蛋白(CHOP)基因蛋白的表达水平。结果与0(对照)、1、10 mmol/L KI染毒组相比,50 mmol/L KI染毒组细胞凋亡率升高(P<0.05);与对照组相比,各染毒组GRP78、IRE1 mRNA表达水平均无统计学差异(P>0.05),CHOP mRNA表达水平升高(P<0.05),GRP78、IRE1和CHOP蛋白表达差异均无统计学意义(P>0.05)。结论内质网应激中IRE1通路可能没有参与高碘诱导的Nthy-ori 3-1细胞凋亡过程。
Objective To investigate the characteristics of IRE1 pathway in thyroid-induced thyroid apoptosis induced by high iodine, and to further analyze the mechanism of thyroid apoptosis induced by high iodine. Methods Nthy-ori 3-1 cells cultured in vitro were treated with 0 (control), 1, 10, 50 mmol / L potassium iodide (KI) and the expression of Nthy-ori 3-1 cells was detected by flow cytometry The expression of GRP78, IRE1 and CHOP gene protein were detected by real-time PCR and Western blot. Results Compared with 0 (control) and 1, 10 mmol / L KI groups, the apoptotic rate of KI group was significantly increased (P <0.05). Compared with the control group, There was no significant difference in the expression of GRP78 and IRE1 (P> 0.05). The expression of CHOP mRNA was increased (P <0.05). There was no significant difference in the expressions of GRP78, IRE1 and CHOP between two groups (P> 0.05). Conclusion The IRE1 pathway in endoplasmic reticulum stress may not participate in the high iodine-induced Nthy-ori 3-1 cell apoptosis.