摘要
为观察束缚应激对二乙基亚硝胺诱发的化学性肝癌大鼠细胞免疫功能的影响,将大鼠随机分为4组:①正常对照组;②化学性肝癌组:以二乙基亚硝胺70 mg/kg灌胃,每周1次,连续8周;③束缚应激组:用绷带束缚大鼠四肢,并将其每只单独装入特制鼠笼限制活动8 h/d,连续18周;④肝癌加应激组:在给二乙基亚硝胺灌胃的同时进行束缚,方法同前。选取第9周、第14周和第19周三个时间点分批处死大鼠,测定各组大鼠腹腔巨噬细胞吞噬功能和脾T细胞产生IFN-γ的能力。结果显示与单纯化学性肝癌组比较,叠加束缚应激的大鼠腹腔巨噬细胞吞噬功能和脾T细胞产生IFN-γ的能力在各时间点均显著降低(P值分别<0.01和<0.05),并且随着束缚时间延长和癌症进展其免疫功能逐渐下降。束缚应激组和化学性肝癌组与正常对照组比较,上述两项指标在各时间点也均有显著降低(P<0.01),并且以早期阶段(0-9周)下降最为显著。说明束缚应激能加重抑制二乙基亚硝胺诱发的化学性肝癌大鼠的细胞免疫功能,这可能是其促进肿瘤发生发展的重要机制。
To investigate the effects of restrain stress on cellular immunity in rats with hepatocarcinoma induced by di-ethylnitrosamine, rats were randomly divided into 4 groups for study in which the first group was set up as normal control . To the second group of rats, 70 mg/kg of diethylnitrosamine were given once a week for 8 weeks. The third group of rats was immobilized with bound feet, 8 hours per day for 18 weeks, were treated with both diethylnitrosamine and immobilization. In each group of rats, the phagocytic function of peritoneal macrophages and the production of IFN-γ in splenic T cells were determined in 9th, 14th and 19th week respectively. The results showed that the phagocytic function of peritoneal macrophages and the production of IFN-γ in the fourth group were significantly lower than those in the second group. Differences between these two groups were notable. Moreover, with the development of hepatocarcinoma and the treatment with immobilization, they became more and more lower, Meanwhile, predominant suppression of phagocytic function and secretion of IFN-γr were detected both in the third and second group in comparison with those of the normal controls and the reduction was more prominent during the early stage (0 - 9 weeks ) . It concludes that restrain stress could aggravate the depression of cellular immunity in rats with experimental hepatocarcinoma and this might be the important mechanism to promote the development of cancer.
出处
《上海免疫学杂志》
CSCD
北大核心
2003年第5期343-345,348,共4页
Shanghai Journal of Immunology
基金
国家中医药管理局科研基金资助项目(No.37600176)
人事部留学回国人员A类重点课题资助项目(2001)
