目的：研究藤黄酸（THS）对实验性动物造血及免疫功能的影响，以验证该药的主要毒副作用。方法：以荷瘤小鼠外周血中白细胞数，正常大鼠体重增长、胸腺及脾脏系数、外周血中白细胞数和骨髓有核细胞数，正常小鼠的血清半数溶血值（HC50）及吞噬指数 等为指标，观察药物的毒副作用。结果：THS iv（8，4，2 ms/kg）对荷瘤小鼠外周血中白细胞总数无明显影响；THS iv（6，3，1.5ms/kS）对正常大鼠外周血中白细胞总数、骨髓有核细胞数、体重、胸腺及脾脏无明显影响；THS iv（8，4，2ms/ks）对小鼠的血清溶血素及巨噬细胞吞噬能力无明显影响。结论：在有效剂量范围内，THS对实验性动物造血功能及免疫功能无明显影响。

目的：观察藤黄酸（gambogic acids, GA）对肝癌细胞凋亡的诱导作用并探讨其分子作用机制。方法与结果：采用MTT比色法检测藤黄酸对人肝癌和人正常肝细胞增殖作用的影响，结果表明，藤黄酸对人肝细胞性肝癌SMMC27721细胞株和QGY27701细胞株有明显增殖抑制作用，并呈剂量依赖性，而对正常人肝组织L202细胞株作用相对较弱；光镜及电镜形态学观察结果显示，给予GA后，肝癌细胞发生明显的细胞凋亡形态学变化，如细胞体积变小，细胞核固缩，出现凋亡小体等；采用RT2PCR和Western blotting方法检测bax mRNA以及bax和p53蛋白表达变化，结果表明GA可诱导bax mR2NA及bax和p53蛋白表达上调；琼脂糖凝胶电泳显示，给予GA后，SMMC-7721裸小鼠移植瘤组织呈现典型的DNA ladder电泳梯状条带。结论：藤黄酸可显著抑制人肝癌细胞的增殖，其分子作用机制可能通过促进bax和p53表达上调，从而诱导人肝细胞性肝癌细胞凋亡。

目的：研究藤黄总酸的体内外抗肿瘤活性。方法：以抑瘤率和生命延长率观察药物的体内抗肿瘤活性，以药物对肿瘤细胞株的抑制率为指标，探讨其体外抗瘤作用。结果：藤黄总酸（8，4，2 mg/kg）iv对Heps、Ec及s180的肿瘤生长具有明显的抑制作用（P<0.01）；ip（1.5，0.75，0.375 mg/kg）能显著延长Heps、EAc、S180腹水型小鼠移植瘤的存活天数；藤黄总酸对人肝癌细胞BEL-7402及人肺腺癌细胞SPC-A1有较强的抑制作用。结论：藤黄总酸对肿瘤细胞的体内外生长有明显抑制作川。

AIM: To investigate the antitumor effect of recombinant L-asparaginase on the growth of several tumors such as P388, L1210, hepatocellular carcinoma (Heps), K562, P815, and sarcoma 180 (S180). METHODS: Tumor cells (K562, L1210, and P815) were cultured in vitro and the morphology of those cells was observed with inverse microscope and transmission electron microscope. MTT assay was performed to measure the cell proliferation and inhibition rate. DNA content was assayed by flow cytometry. According to protocols of transplant tumor research, mice were transplanted with tumor cells LI210, P388, Heps, and S180. The survival rate and weight of tumor were observed after the treatment of test drugs. RESULTS: The antimmor effects of L-asparaginase were observed in vitro with tumor cells K562, L1210, and P815 (P<0.01). In vivo experiments showed that ip adminis-tration of L-asparaginase significantly increased the survival rate and life span of mice with P388 or LI210 tumor cells (P<0.01). Tumor growth induced with Heps was also significantly suppressed. Furthermore, significant suppression of tumor growth was observed in mice induced with Heps and S180 by iv administration of L-asparaginase. CONCLUSION: Recombinant L-asparaginase markedly inhibited tumors tested in this study and the results strongly suggest that recombinant L-asparagiuase has great potential for clinical treatment of these tumors.

is on nude mice xenografts was observed by Annexin-V/PI doubling staining flow cytometry assay and DNA fragmentation assay. To further determine the molecular mechanism of apoptosis induced by GA, the changes on the expression of bcl-2 and bax genes were detected by RT-PCR. RESULTS: After incubation with GA, low differential human gastric cancer line BGC-823 was dramatically inhibited in a dose-dependent manner. After these cells were exposed to GA for 24, 48 and 72 h, the IC50 value was 1.02±0.05, 1.41±0.20 and 1.14±0.19 μmol/L, respectively. Apoptosis in BGC-823 cells induced by GA was observed by Annexin-V/PI doubling staining flow cytometry assay. The apoptotic population of BGC-823 cells was about 12.96% and 24.58%, respectively, when cells were incubated with 1.2 μmol/L GA for 48 and 72 h. T/C (%) of human gastric carcinoma adenocarcinoma BGC-823 nude mice xenografts was 44.3, when the nude mice were treated with GA (8 mg/kg). Meanwhile, apoptosis induced by GA was observed in human gastric carcinoma adenocarcinoma BGC-823 nude mice xenografts. The increase of bax gene and the decrease of bc1-2 gene expressions were found by RT-PCR. CONCLUSION: The inhibition of GA on human gastric cancer line BGC-823 was confirmed. This effect connects with the inducing apoptosis in BGC-823 cells and the molecular mechanism might be related to the reduction of expression of apoptosis-regulated gene bcl-2, and the improvement of the expression of apoptosis-regulated gene bax. The result was also confirmed in vivo.