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Ｌ６１５可移植性白血病细胞经冻融，离心处理后，其上清液注入小鼠体内可诱导产生低分子生物抗癌活性物质。当其作用于Ｌ６１５白血病小鼠后，可使３３％的小鼠平均生存期由６ｄ延长到１５０ｄ，平均生命延长率达到２５２７．８％。用ＩＬ─２／ＬＡＫ细胞作用后的白血病小鼠，其平均生存期仅延长到１１ｄ。在上述基础上，分别将中药有效成份小蘖胺、黄芪多糖和当归多糖同低分子抗癌物质有机地配合作用于白血病小鼠后，有７５％的小鼠生存期达到了２７５ｄ，生命延长率提高了２０６１％。外周血及脏器组织未发现典型的白血病细胞侵润，骨髓细胞中１９号染色体上Ｂｊ白血病携带频率由对照组的４７．５％下降到０。此外，小蘖胺，黄芪多糖和当归多糖皆在不同程度上诱导小鼠脾脏细胞活化产生ＬＡＫ细胞。在体外实验中，其ＬＡＫ细胞对￣（１２５）Ｉ标记的白血病细胞的最大杀伤活性与ＩＬ－２在体外诱导产生的ＬＡＫ细胞活性相比较，可达到ＩＬ─２剂量提高２０倍时产生的杀伤效应。同时上述中药有效成分都在不同程度上使小鼠肝胆组织ＳＯＤ活性显著增强，阻遏了环磷酰胺对ＳＯＤ的抑制作用，逆转了环磷酰胺对正常脾脏免疫细胞的抑制和破坏作用。
L615 transplantable leukemia cells were freeze-thawed and centrifuged. After the supernatant was injected into mice, low molecular biological anticancer active substances could be induced. When it was applied to L615 leukemia mice, the average survival time of 33% mice could be extended from 6 days to 150 days, and the average life extension rate was 2528.8%. The average survival time of leukemic mice treated with IL-2/LAK cells was only extended to 11 days. On the basis of the above, 75% of the mice had a survival period of 275 days, and the life prolongation rate was achieved after organically cooperating Berberine, astragalus polysaccharides, and angelica polysaccharides together with low-molecular-weight anti-cancer substances in leukemia mice. Increased 2061%. No typical leukemia cell infiltration was found in peripheral blood and organ tissues. Bj leukemia carrying frequency on chromosome 19 in bone marrow cells decreased from 47.5% in the control group to 0. In addition, berberine amine, astragalus polysaccharide and angelica polysaccharide all induced mouse spleen cells activation to produce LAK cells to varying degrees. In vitro, the LAK cell’s maximal cytotoxic activity against 125I-labeled leukemia cells was comparable to IL-2-induced LAK cell activity in vitro, which resulted in killing when the IL-2 dose was increased 20-fold. effect. At the same time, the active ingredients of the above-mentioned traditional Chinese medicines have significantly enhanced SOD activity in the liver and gallbladder tissues of mice, inhibited the inhibitory effect of cyclophosphamide on SOD, and reversed the inhibitory and destructive effects of cyclophosphamide on normal spleen immune cells.