摘要
目的探讨雌激素E2(estradiol,E2)对原发性肝癌发生发展的影响,及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。方法选取南方医科大学南方医院2013年1月~2014年6月接收的原发性肝癌男性患者作为观察组,同期接收的非原发性肝癌患者为正常对照组。采用ELISA法检测2组患者血清中的E2、IL-1β和VEGF浓度,Western blot法检测2组肝组织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)浓度均明显高于正常对照组,2组间比较差异有统计学意义(P<0.01);观察组肿瘤组织中E2R和IL-1βR蛋白表达水平均明显高于正常对照组,2组间比较差异有统计学意义(P<0.01)。结论 E2对原发性肝癌的发生发展具有促进作用,其作用机制可能是通过上调IL-1/IL-1βR通路,促进VEGF的表达,从而促进肿瘤血管的形成。
Objective To investigate whether estrogen E2( estradiol,E2) promotes the development of primary liver cancer,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 Male patients with primary liver cancer were selected as the observation group of our hospital from January 2013 to June 2014. The same period of non-primary liver cancer patients were selected as normal control group,the patients were detected by ELISA,and serum E2,IL-1β and VEGF concentrations were detected by Western blot in liver tumor tissue and normal liver tissue and IL-1βR E2 R protein levels. Results Serum in E2,IL-1β,and vascular endothelial in observation group( vascular endothelial growth factor,VEGF) were significantly higher than the normal control group,and between the two groups was significant difference( P < 0. 01); expressions of E2 R and IL-1βR in tumor tissue of obsenvation group 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 of tumor blood vessels and completed.
出处
《中国生化药物杂志》
CAS
北大核心
2014年第6期21-23,共3页
Chinese Journal of Biochemical Pharmaceutics
基金
国家自然科学基金(81172267)
