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目的观察淫羊藿苷(icariin,ICA)对CIK杀伤子宫内膜癌耐药细胞株的影响,初步探讨其作用机制。方法 MTT检测ICA对子宫内膜癌耐药细胞株B-MD-C1(ADR+/+)的增殖抑制作用;流式细胞术(FCM)检测ICA对肿瘤细胞周期分布和凋亡的影响;乳酸脱氢酶释放法(LDH)法检测CIK(细胞因子诱导的肿瘤杀伤细胞)对ICA处理前后肿瘤细胞的杀伤作用。RT-PCR法和流式细胞术检测肿瘤细胞表面粘附因子CD18和CD54基因和蛋白表达的影响。结果 12.5~50μg/ml ICA对B-MD-C1(ADR+/+)细胞活力和凋亡没有明显影响。100μg/ml ICA能明显抑制B-MD-C1(ADR+/+)细胞的增殖(P<0.01),且可诱导其凋亡。经0~100μg/ml ICA处理12 h后,S期细胞明显增加(P<0.01)。经12.5~50μg/ml ICA处理12 h后,B-MD-C1(ADR+/+)细胞CD18和CD54基因和蛋白表达均增加,且对CIK细胞的杀伤敏感性增强,呈现ICA浓度依赖性。结论 12.5~50μg/ml ICA增加了B-MD-C1(ADR+/+)细胞对CIK的杀伤敏感性,与ICA诱导肿瘤细胞CD18和CD54表达增加有关。
Objective To investigate the effect of icariin (ICA) on CIK-resistant endometrial carcinoma cell line, and to explore its mechanism. Methods The inhibitory effect of ICA on the proliferation of endometrial carcinoma cell line B-MD-C1 (ADR + / +) was detected by MTT assay. The effect of ICA on the cell cycle distribution and apoptosis was detected by flow cytometry (FCM) The killing effect of CIK (cytokine-induced tumor killer cells) on tumor cells before and after ICA treatment was detected by the method of LDH. RT-PCR and flow cytometry were used to detect the expression of adhesion molecules CD18 and CD54 on tumor cells. Results ICA at 12.5 ~ 50μg / ml had no significant effect on the viability and apoptosis of B-MD-C1 (ADR + / +) cells. ICA at 100μg / ml significantly inhibited the proliferation of B-MD-C1 (ADR + / +) cells (P <0.01) and induced its apoptosis. After being treated with 0-100 μg / ml ICA for 12 h, the number of S phase cells increased significantly (P <0.01). After treated with 12.5 ~ 50μg / ml ICA for 12 h, the expression of CD18 and CD54 gene and protein in B-MD-C1 (ADR + / +) cells increased and the cytotoxicity to CIK cells increased. Conclusion ICA at 12.5 ~ 50μg / ml increases the cytotoxicity of CIK against B-MD-C1 (ADR + / +) cells, which is related to the increase of CD18 and CD54 expression induced by ICA.