如何发挥中医药优势，与西医治疗紧密结台，以提高肝癌的临床疗效一直是我国肝癌防治研究的重要课题。本文结台国内外研究成果及我们自己的研究实践，对中医药防治肝癌的特色、优势及面临的问题做～概要的分析，旨在促进进一步深人研究。

目的：比较乙甲斑蝥素缓释注射剂型与普通注射液肝脏注射的急性毒性，为缓释剂型的临床肝脏注射应用提供实 验依据方法：60只小鼠及18只大鼠备随机分为3组。分别肝脏注射等量击甲斑蝥素缓释溶液、普通水剂及药物缓释辅料泊洛沙姆407溶被。观察小鼠行为状态、生存情况及大鼠肝脏病理形志学变化。结果：注射去甲斑蝥素缓释藩渣组小鼠死亡率低于普通艰溶液组；泊洛抄姆407小鼠肝脏注射的LD5n>625mg、kg；缓释制剂对注射部位肝脏的刺激毒性鞍普通错剂大。坏死范围广。结论：去甲斑螫素缓释错剂肝脏注射毒性低于普通制剂，缓释制荆肝肿瘤内注射安全、可行。

To search for a new clinical application of melittin (Mel): treating hepatocellular carcinoma with Mel gene. Methods: Recombinant adenoviruses carrying the Mel gene and a-fetoprotein (AFP) promoter (Ad-rAFP-Mel) were constructed through a bacterial homologous recombinant system. The efficiency of adenovirus-mediated gene transfer and the inhibitory effect of Ad-rAFP-Mel on the proliferation of hepatocarcinoma cells were determined by X-gal stain and MTT assay, respectively. The tumorigenicity of hepatocarcinoma cells transfected by Ad-rAFP-Mel and the antitumor effect of Ad-rAFP-Mel on transplanted tumor in nude mice were detected in vivo. Results: The Mel mRNA was transcribed in BEL-7402 hepatocellular carcinoma cells transducted by Ad-rAFP-Mel. The efficiency of adenovirus-mediated gene transferred to BEL-7402 cells was 100% when the multiplicity of infection of Ad-rAFP-Mel was 10 in vitro, and was also high in vivo. The inhibitive rates of Ad-rAFP-Mel and Ad-rAFP for BEL7402 cells were 66.2

The eVects of glucocorticoid (GC) hormones are mediated via an intracellular receptor, the glucocorticoid receptor (GR). It has been established that glucocorticoid down-regulate GR. Ginsenosides (GSS) from extract of Panax ginseng have demonstrated glucocorticoid-like activities in homeostasis and regulation of immunity, etc. We hypothesize that ginsenosides might mediate some of their actions by binding to the GR. The present study is aimed to determine whether GSS can act like a GC analog in the activation of glucocorticoid response element-luciferase activity in HL7702 cells. We found that GSS alone had no eVect on the expression of reporter gene, but it enhanced dexamethasone (Dex)-induced transcription of reporter gene. To further explore the eVects of GSS, we examined the inXuence of GSS on the gene and protein expression as well as hormone binding activity of GR by semi-quantitative RT-PCR, Western blot, and radioligand-binding assay, respectively. GSS partially reversed the Dex-induced decrease in GR expression and hormone binding activity with an optimal dose of 25 g/ml, implicating a positive regulatory eVect of GSS on GR expression and binding activity. Therefore, our result suggests that GSS may reverse partially the dexamethasone-induced down-regulation of glucocorticoid receptor