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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 observe the effect of restraint stress on the cellular immune function of chemical hepatocarcinoma induced by diethylnitrosamine in rats, the rats were randomly divided into four groups: ① normal control group; ②chemic liver cancer group: Nitramine 70 mg / kg orally, once a week for 8 weeks; ③ restraint stress group: the bandage tethered rat limbs, and each of them into a special squirrel cage restricted activity 8 h / d, continuous 18 weeks; ④ Hepatocellular carcinoma plus stress group: In the same time as the administration of diethylnitrosamine gavage, the same way. The rats were sacrificed in batches at the 9th, 14th and 19th week. The phagocytosis of peritoneal macrophages and the ability of spleen T cells to produce IFN-γ were measured. The results showed that the phagocytic function of peritoneal macrophages and the ability of spleen T cells to produce IFN-γ were significantly decreased at each time point (P <0.01 and <0.05, respectively) , And its immune function gradually declines with the prolonged binding and cancer progression. Compared with the normal control group, the above two indexes also significantly decreased (P <0.01) in the restraint stress group and the chemical liver cancer group, and decreased most significantly in the early stage (0-9 weeks). These results suggest that restraint stress can aggravate the cellular immune function of rats induced by diethylnitrosamine, which may be one of the important mechanisms that promote the tumorigenesis.