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脂质体干扰素α对小鼠Lewis肺癌转移及脾细胞增殖的影响 被引量:4

Effects of Interferon-α Liposome on Lung Metastasis of Lewis Lung Carcinoma and Proliferation of Splenocytes in Mice
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摘要 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(IF-α),连续10d;测小鼠肺湿重、肺转移给节数和ConA诱导的脾细胞DNA参入量。结果IFN-α5×104、20×104U/kg组,小鼠肺湿重较对照组减少14.1%、19.6%,肿瘤肺转移结节数减少32.7%、50.0%,ConA刺激的脾细胞DNA参入量增加24.6%、46.8%。1/10剂量的L-IFN-α可产生相同的药理活性。小鼠环磷酰胺50mg/kgip3d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肺癌肺转移,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。 C57BL/6N mice were administrated iv with Lewis lung carcinoma cells, and then ip interferon-α liposome (L-IFN-α) or interferon-α (IFN-α) for ten days. The lung weight, metastasis foci and proliferation of splenocytes in mice were observed.The results showed that IFN-α inhibited the lung metastasis of Lewis lung carcinoma and increased proliferation of splenocytes in mice. ip 1 ~20 ×104U/kg of IFN-α for 10d, lung weight of thece decreased by 3. 1 % ~ 18. 8 %, the numbers of metastasis foci decreased by 8. 2 %~49. 9 %, and [3H]TdR incorporation increased by 1. 8 % ~46.7 %. After envelopment of IFN-α by liposome, its potency of anti-lung-metastasis of Lewis lung carcinoma and promoting proliferation of splenocytes increaed 11 times as against unenveloped IFN-α. L-IFN-αhad a more powerful effects of anti-metastasis and increasing proliferation of splenocytes in the mice administrated previously with cyclophosphamide than in the unadministrated mice. These results indicated that IFN-α liposome is a prospective preparation.
出处 《中国生化药物杂志》 CAS CSCD 1997年第4期174-177,共4页 Chinese Journal of Biochemical Pharmaceutics
关键词 脂质体 干扰素Α 肺癌 肿瘤转移 脾细胞 Liposome, Interferon-α,Lewis lung carcinoma, Neaplansma metastasis, Splenocytes
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  • 1Giuseppe Masucci,Peter Ragnhammar,Peter Wers?ll,H?kan Mellstedt. Granulocyte-monocyte colony-stimulating-factor augments the interleukin-2-induced cytotoxic activity of human lymphocytes in the absence and presence of mouse or chimeric monoclonal antibodies (mAb 17-1A)[J] 1990,Cancer Immunology Immunotherapy(4):231~235

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