性激素通過IL-1_IL-1R通路促进原发性肝癌的机制的研究性激素通过IL-1_IL-1R通路促进原发性肝癌的机制的研究.docVIP

修改意见： 性激素通过IL-1/IL-1R通路促进原发性肝癌的机制的研究 [摘要]目的 探讨雌激素E2(Estradiol，E2)是否对原发性肝癌的发生发展有促进作用，以及该作用机制是否通过白细胞介素-1(Interleukin-1，IL-1)/白细胞介素-1受体（Interleukin-1 receptor，IL-1R）通路。方法 选取我院2013年1月至2014年6月接收的原发性肝癌男性患者作为观察组，选取同期接收的非原发性肝癌患者作为正常对照组，分别采用ELISA法检测两组患者血清中的E2、IL-1β和VEGF浓度，采用Western blot法检测两组肝肿瘤组织和正常肝组织中E2R和IL-1βR蛋白表达水平。结果 观察组患者血清中E2、IL-1β和血管内皮生长因子(Vascular Endothelial Growth Factor，VEGF)浓度显著性高于正常对照组，且两组间比较具有显著性差异（P0.01）；观察组肿瘤组织中E2R和IL-1βR蛋白表达水平显著性高于正常对照组，且两组间比较具有显著性差。异（P0.01）。结论 E2对原发性肝癌的发生发展具有促进作用，且改作用机制可能是通过上调IL-1/IL-1βR通路，促进VEGF的表达，引起肿瘤血管的形成而完成的。 [关键词] 雌激素；白细胞介素-1；白细胞介素-1受体；原发性肝癌 [中图分类号] TQ460. 7 [文献标识码]A Mechanism of primary liver cancer promoting hormone pathway through IL-1/IL-1R [Abstract] Objective To investigate whether estrogen E2 (Estradiol, E2) for the development of primary liver cancer are promoted, as well as the mechanism of action is through interleukin -1 (Interleukin-1, IL-1) / IL 1 receptor (Interleukin-1 receptor, IL-1R) pathway. Methods Selected male patients with primary liver cancer as the observation group of our hospital from January 2013 to June 2014. Selected the same period of non-primary liver cancer patients as normal control group, the patients were detected by ELISA serum E2, IL-1β and VEGF concentrations were detected by Western blot in liver tumor tissue and normal liver tissue and IL-1βR E2R protein levels. Results Serum observation group E2, IL-1β, and vascular endothelial growth factor (Vascular Endothelial Growth Factor, VEGF) were significantly higher than the normal control group, and between the two groups was significant difference (P 0.01); Observer Group E2R tumor tissue and IL-1βR protein levels were significantly higher than the normal control group, and between the two groups was significant difference (P 0.01). Conclusion The development of E2 to promote the role of primary liver cancer, and the mechanism of action may be changed by upregulating IL-1/IL-1βR pathway promotes the expression of VEGF, causing the formation