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Ｃ５７ＢＬ／６Ｎ小鼠尾静脉注射Ｌｅｗｉｓ肺癌细胞后，腹腔注射脂质体干扰素α（Ｌ－ＩＦＮ－α）和未包裹干扰素α（ＩＦＮ－α），连续１０ｄ；测小鼠肺湿重、肺转移结节数和ＣｏｎＡ诱导的脾细胞ＤＮＡ掺入量。结果ＩＦＮ－α５、２０万ｕ·ｋｇ（－１）组，小鼠肺湿重较对照组减小１４．１、１９．６％，肿瘤肺转移结数减少３２．７、５０．０％，ＣｏｎＡ刺激的脾细胞ＤＮＡ掺入量增加２４．６、４６．８％。１／１０剂量的Ｌ－ＩＦＮ－α可产生相同的药理活性。小鼠环磷酸胺５０ｍｇ·ｋｇ（－１）ｉｐ３ｄ后，尾静脉注射瘤细胞，实验处理同上。结果Ｌ－ＩＦＮ－α和ＩＦＮ－α对环磷酰胺处理小鼠的Ｌｅｗｉｓ肺癌细胞肺转移的抑制作用更为明显。本文结果表明，ＩＦＮ－α可抑制小鼠Ｌｅｗｉｓ肺癌转移，促进ＣｏｎＡ刺激的脾细胞增殖，并与剂量明显相关。脂质体包裹ＩＦＮ－α可使其生物活性提高约１０倍。对免疫功能受抑小鼠作用更为显著。
After Lewis lung cancer cells were injected into tail vein of C57BL/6N mice, liposomal interferon-alpha (L-IFN-α) and unencapsulated interferon-α (IFN-α) were injected intraperitoneally for 10 days. The mice lung wet weight was measured. Number of pulmonary metastatic nodules and conA-induced splenocyte DNA incorporation. RESULTS: In the IFN-α5 and 200,000 u·kg(-1) groups, the wet weight of lungs in mice was reduced by 14.1 and 19.6% compared with the control group, and the number of metastatic lung metastases was reduced by 32.7 and 50.0%. ConA-stimulated splenocyte DNA incorporation increased by 24.6 and 46.8%. A 1/10 dose of L-IFN-α produces the same pharmacological activity. After the mouse cyclic phospho-amine 50 mg·kg(-1)ip3d, the tumor cells were injected into the tail vein and the experimental treatment was the same as above. Results The inhibitory effect of L-IFN-α and IFN-α on lung metastasis of Lewis lung cancer cells treated with cyclophosphamide was more obvious. The results of this study indicate that IFN-α can inhibit Lewis lung cancer metastasis and promote the proliferation of ConA-stimulated splenocytes, and is significantly related to the dose. Liposome encapsulation of IFN-α can increase its biological activity by about 10 fold. The effect on immune function suppressed mice is even more pronounced.