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NIS、VEGF-A和甲状腺自身抗体在伴或不伴桥本氏病的甲状腺乳头状癌中的表达

Expression of NIS, VEGF-A and Thyroid Autoantibody in Papillary Thyroid Carcinoma with or without Hashimoto's Disease.

作者信息

Ma Ye, He Junyi, Shen Na, Guo Ruosheng

机构信息

Department of Surgery, Jiading District Central Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.

Department of Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.

出版信息

ORL J Otorhinolaryngol Relat Spec. 2019;81(5-6):281-286. doi: 10.1159/000501620. Epub 2019 Sep 3.

Abstract

BACKGROUND

Since the incidence of papillary thyroid carcinoma (PTC) combined with Hashimoto's thyroiditis (HT) has increased year by year, but the mechanism is still unknown, the goal of this study was to investigate the expression of Na+/I- symporter (NIS), vascular endothelial growth factor (VEGF)-A and thyroid autoantibodies in HT combined with PTC, and to explore the relationship between HT and PTC.

METHODS

Real-time fluorescence quantitative polymerase chain reaction was used to detect the expression of VEGF-A and NIS in 38 cases of PTC and HT combined with PTC and in 20 cases of normal tissues; preoperative serum TPOAb and TgAb levels in each group were detected by ELISA.

RESULTS

The expression of VEGF-A in PTC and HT combined with PTC was significantly higher than that in normal tissues (p < 0.05), and the expression of VEGF-A in HT combined with PTC was higher than that in PTC (p < 0.05). The expression of NIS mRNA in PTC and HT combined with PTC was significantly decreased compared to that in normal tissues (p < 0.05), and NIS mRNA in HT combined with PTC tissue was lower than that in PTC tissue (p < 0.05). The preoperative levels of TPOAb and TgAb in the HT combined with PTC group were higher than those in the normal group and the PTC group (p < 0.05).

CONCLUSION

The presence of HT may inhibit iodine uptake and cause a decrease in NIS. Increased levels of TPOAb and TgAb in HT patients lead to a high expression of TSH and stimulate VEGF secretion. This may explain why HT could accelerate the occurrence and development of PTC.

摘要

背景

由于甲状腺乳头状癌(PTC)合并桥本甲状腺炎(HT)的发病率逐年上升,但机制仍不清楚,本研究的目的是调查HT合并PTC中钠/碘同向转运体(NIS)、血管内皮生长因子(VEGF)-A和甲状腺自身抗体的表达,并探讨HT与PTC之间的关系。

方法

采用实时荧光定量聚合酶链反应检测38例PTC及HT合并PTC患者和20例正常组织中VEGF-A和NIS的表达;采用酶联免疫吸附测定法检测每组术前血清甲状腺过氧化物酶抗体(TPOAb)和甲状腺球蛋白抗体(TgAb)水平。

结果

PTC及HT合并PTC中VEGF-A的表达显著高于正常组织(p<0.05),HT合并PTC中VEGF-A的表达高于PTC(p<0.05)。与正常组织相比,PTC及HT合并PTC中NIS mRNA的表达显著降低(p<0.05),HT合并PTC组织中NIS mRNA低于PTC组织(p<0.05)。HT合并PTC组术前TPOAb和TgAb水平高于正常组和PTC组(p<0.05)。

结论

HT的存在可能抑制碘摄取并导致NIS降低。HT患者TPOAb和TgAb水平升高导致促甲状腺激素高表达并刺激VEGF分泌。这可能解释了HT为何能加速PTC的发生和发展。

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