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鼻咽癌患者胆汁酸循环紊乱促进白细胞介素-10分泌升高。

Bile acids cycle disruption in patients with nasopharyngeal carcinoma promotes the elevation of interleukin-10 secretion.

作者信息

Wang Cheng-Shi, Liu Shou-Hou, Peng Jin, Tang Chen, Zhu Wei-Guo

机构信息

Department of Radiotherapy, Lianshui People's Hospital, Huai'an, Jiangsu, 223400, China.

Department of otorhinolaryngology,Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, 223300, China.

出版信息

Afr Health Sci. 2015 Dec;15(4):1200-3. doi: 10.4314/ahs.v15i4.19.

Abstract

BACKGROUND

Unclear pathogenesis existed for nasopharyngeal carcinoma.

AIMS

to analyze the role of bile acids in the pathogenesis of nasopharyngeal carcinoma.

METHODS

20 healthy volunteers and 20 patients with nasopharyngeal carcinoma were enrolled between January 1(st), 2013 and December 31(st), 2014. ESI-QTOF-MS analysis of serum was performed to find altered bile acids components. The biological function of changed bile acids was investigated using in vitro experiment.

RESULTS

Compared with healthy volunteers, the level of DCA and GDCA exhibited higher abundance in patients with nasopharyngeal carcinoma (p<0.01). Furthermore, the biological function was investigated for the inhibition of DCA and GDCA towards the secretion of IL-10 by CD4+CD25- T cells. Both DCA and GDCA significantly inhibited the secretion of IL-10 by CD4+CD25- T cells. Furthermore, DCA+GDCA can show stronger inhibition towards the secretion of IL-10 than DCA and GDCA.

CONCLUSION

The inhibition of IL-10 secretion by elevated DCA and GDCA components in nasopharyngeal carcinoma patients is the inducer for nasopharyngeal carcinoma.

摘要

背景

鼻咽癌的发病机制尚不清楚。

目的

分析胆汁酸在鼻咽癌发病机制中的作用。

方法

2013年1月1日至2014年12月31日期间招募了20名健康志愿者和20名鼻咽癌患者。对血清进行电喷雾电离-四极杆飞行时间质谱(ESI-QTOF-MS)分析以发现胆汁酸成分的改变。使用体外实验研究变化的胆汁酸的生物学功能。

结果

与健康志愿者相比,鼻咽癌患者中脱氧胆酸(DCA)和甘氨脱氧胆酸(GDCA)的水平表现出更高的丰度(p<0.01)。此外,研究了DCA和GDCA对CD4+CD25-T细胞分泌白细胞介素-10(IL-10)的抑制作用的生物学功能。DCA和GDCA均显著抑制CD4+CD25-T细胞分泌IL-10。此外,DCA+GDCA对IL-10分泌的抑制作用比DCA和GDCA更强。

结论

鼻咽癌患者中升高的DCA和GDCA成分对IL-10分泌的抑制是鼻咽癌的诱导因素。

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