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目的研究氨氯地平对小鼠黑色素细胞瘤B16细胞自发性肺转移的抑制作用及其机制。方法将小鼠黑色素细胞瘤B16细胞接种于C57BL/6J小鼠右腹股沟皮下,2×106个/只,次日将小鼠随机分为阴性对照组(给予生理盐水0.2 ml/只,每天灌胃1次,共21 d)、氨氯地平低、中、高剂量组(分别给予氨氯地平1、3和10 mg/kg,每天灌胃1次,共21 d)和环磷酰胺组(给予环磷酰胺20 mg/kg,每2 d腹腔注射1次,共7次),观察小鼠成瘤及活动情况。于末次给药后第2天断颈处死小鼠,观察小鼠的肺转移情况及抑瘤率;体外进行血小板聚集试验及黏附试验,比较药物作用前后血小板聚集及黏附能力的差异。结果氨氯地平可抑制小鼠黑色素细胞瘤B16细胞的体内增殖、自发性肺转移、B16细胞诱导的小鼠血小板聚集以及血小板与B16细胞的黏附,且呈剂量依赖性。结论氨氯地平对小鼠黑色素细胞瘤B16细胞具有抑制体内增殖和自发性肺转移的作用,其机制可能与抑制肿瘤细胞诱导的血小板聚集及肿瘤细胞与血小板的黏附有关。
Objective To study the inhibitory effect of amlodipine on the spontaneous lung metastasis of mouse melanoblastoma B16 cells and its mechanism. Methods Mouse melanocytoma B16 cells were inoculated into the right inguinal of C57BL / 6J mice subcutaneously at a dose of 2 × 10 6 cells / day. The mice were randomly assigned to the negative control group (0.2 ml / normal saline) 1, a total of 21 d), amlodipine low, medium and high dose groups (given amlodipine 1, 3 and 10 mg / kg orally daily for 21 days) and cyclophosphamide Cyclophosphamide 20 mg / kg, intraperitoneal injection every 2 days, a total of 7 times), observed tumor formation and activity in mice. Mice were sacrificed on the second day after the last administration, lung metastasis and tumor inhibition rate were observed. In vitro platelet aggregation test and adhesion test were conducted to compare the difference of platelet aggregation and adhesion capacity before and after drug administration. Results Amlodipine can inhibit the proliferation of mouse melanoblastoma B16 cells in vivo, spontaneous lung metastasis, platelet aggregation induced by B16 cells and platelet adhesion to B16 cells in a dose-dependent manner. Conclusion Amlodipine can inhibit the proliferation and spontaneous lung metastasis of mouse melanoblastoma B16 cells in vitro. The mechanism may be related to the inhibition of tumor cell-induced platelet aggregation and the adhesion of tumor cells and platelets.