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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 observe the effect of anti-inflammatory treatment on the progression of primary hepatocellular carcinoma induced by diethylnitrosamine (DEN). Methods Forty-two rats were selected to establish DEN-induced hepatocellular carcinoma (HCC) model and randomly divided into three groups. The number of hepatic nodules and the changes of hepatic structure in each group were observed at different periods. The expressions of CD68, CD206 and CD34 The expression of TNF-α, IL-10, TGF-β, HGF and NFκB in liver tissues were detected by western blot. Results Compared with the control group and the glucurolactone group, the number of nodules in hydrocortisone group was less, the appearance of liver cancer was later, and the expression of CD68, CD206 and CD34 in liver tissue was less. The relative expression of TNF-α, IL10, TGFβ, HGF and NFκB in liver tissue was less in 8 ~ 12 weeks. Conclusion Inhibition of monocyte-macrophage-mediated chronic nonspecific inflammation in the liver microenvironment can delay the progression of DEN-induced primary hepatocarcinoma at the early stages of cancer induction.