中文摘要：

目的：探讨健脾解毒方延长脾虚肝癌模型大鼠带瘤生存及与MHCⅠ/MHCⅡ的关系。方法：105只雄性Wistar大鼠随机分为空白对照组、肝癌模型组、脾虚模型组、脾虚肝癌模型组、胸腺五肽组及健脾解毒方低、高剂量组,进行造模和干预。实验中记录动物的体质量、生存时间、肝癌大鼠濒死状态时恶液质积分并采集标本。免疫组化与Western blot方法检测大鼠肝组织及肝癌组织MHCⅠ/MHCⅡ分子表达。结果：健脾解毒方高剂量组和胸腺五肽组累积生存率高于其余各组（P〈0.05）,且其恶液质评分低于其余各组（P〈0.05）。各造模组中,MHCⅠ分子在肝组织中的表达水平高于癌组织,肝组织和癌组织中均以健脾解毒方高剂量组表达最强（P〈0.01）。MHCⅡ分子在癌组织表达强于肝组织,肝组织中以健脾解毒方高剂量组表达最强（P〈0.01）,癌组织中以脾虚肝癌组表达最强（P〈0.01）。结论：健脾解毒方能对抗移植瘤导致的恶液质的发生和进展,显著延长荷瘤鼠的生存时间,其作用可能与上调MHCⅠ/MHCⅡ有关。

英文摘要：

Objective：To explore that Invigorating Spleen and Detoxification Decoction（ISD） enhanced the survival of spleen-deficiency liver cancer rats and the effect on major histocompatibility complex Ⅰ （ MHC Ⅰ ） and major histocompatibility complex Ⅱ （ MHC Ⅱ ）. Methods ：105 male Wistar rats were randomly divided into blank control group,liver cancer model group, spleen-deficiency model group, spleen-deficiency liver cancer model group, Thymopentin group and spleen-deficiency liver cancer model groups treated by low and high-concentration ISD for modeling and intervention. Recorded the animals＇ weight, smvival time, moribund state and cachexia score of liver cancer rats, and collected specimens in the experiment. Immunohistochemistry and Western blot were used to detect MHC Ⅰ/MHC Ⅱ expression in liver tissue and liver cancer tissue. Results：The cumulative survival of high concentration ISD group and Thy- mopentin group were higher than that of the other groups （P 〈 0. 05 ） , and whose cacbexia score were lower than the rest （P 〈 0. 05 ）. In the spleen-deficiency liver cancer model groups,MHC Ⅰ expression in liver tissue was higher than that in liver cancer tissue,both in these two tissues,expression of high-concentration ISD group was the strongest （ P 〈 0. 01 ）. MHC Ⅱ expression in liver cancer tissue was stronger than that in liver tissue, expression of high-concentration ISD group was the strongest in liver tissue,but in liver cancer tissue,the spleen-deficiency liver cancer model group was the strongest （P 〈 0. 01 ）. Conclusion： ISD can significantly decrease the progression of cachexia caused by transplantable tumor and prolong the survival time ,the effect may be related to increasing MHC Ⅰ/MHC Ⅱ expression.