抗炎治疗影响DEN诱导原发性肝癌进展的研究

The effect of anti-inflammatory treatment on the progress of diethylnitrosamine induced primary liver cancer

目的观察抗炎治疗对二乙基亚硝胺(diethylnitrosamine,DEN)诱导原发性肝癌进展的影响。方法选取42只大鼠建立DEN诱导肝癌模型,随机分为3组,观察诱癌不同时期各组肝组织结节个数及肝组织结构的变化,用免疫组化检测3组CD68、CD206和CD34的阳性细胞表达,用western blot检测3组肝组织中TNF-α、IL10、TGF-β、HGF及NFκB等蛋白的相对表达。结果与对照组及葡醛内酯组相比,氢化可的松组结节个数更少,肝癌出现时间更晚,肝组织中CD68、CD206和CD34的阳性细胞表达更少,在诱癌第8~12周TNF-α、IL10、TGFβ、HGF和NFκB等蛋白在肝组织中的相对表达更少。结论抑制肝脏微环境中单核-巨噬细胞介导的慢性非特异性炎症能在诱癌早期延缓DEN诱导原发性肝癌的进展。

Objective To investigate the influence of anti-inflammatory treatment on the progress of DEN induced primary liver cancer. Methods 42 rats which were fed with Diethylnitrosamine（DEN）solution to induce the rat model of liver cancer, and randomly divided into 3 groups. The nodule number and the structural change of liver tissue in each group were observed. CD68, CD206 and CD34 positive expression in liver tissue were detected by immunohistochemical staining in each group. Relative expression of TNF- α,IL10, TGF- β, HGF and NFκB in the liver tissue was detected by western blot in each group. Results Compared with the control group and glucurolactone group,hydrocortisone group’s nodule number was fewer,the appearance time of liver cancer was postponed, the positive expression of CD68, CD206 and CD34 was fewer, the protein relative expression of TNF- α, IL10, TGF- β, HGF and NF kappa B was fewer at the 8th,10 th, and 12 th week. Conclusion Inhibiting the chronic nonspecific inflammation which is mediated by mononuclear- macrophage in liver microenvironment can delay the progress of the primary liver cancer in rats at an early stage which is induced by DEN.