YIGSR聚合衍生物对B16黑色素瘤细胞实验性肺转移的抑制作用

摘要

目的：研究Tyr－Ile－Gly－Ser－Arg（YIGSR）均叉、杂叉 聚合肽的抗肿瘤转移作用。方法：观察药物对B16黑色素瘤细胞 实验性肺转移的影响。结果：尾静脉接种B16黑色素瘤细胞第2 1天，46例对照组和实验组小鼠肺转移瘤灶形成比例100％。10例 对照组小鼠平均肺转移结节数1055±782。与瘤细胞共注射 的适宜剂量YIGSR均叉、杂叉肽可明显降低实验组小鼠的肺转移 结节数，并呈一定的剂量依赖关系。其中，100μg～200μgYIGSR 均叉和同剂量杂叉肽组肺转移结节数与对照组比较，P<0.05和P< 0.01；50μg均叉肽与对照组比较，P<0.05。但受试合成肽未明显 降低已形成肺转移小鼠的肺脏重量。结论：YIGSR聚合衍生物有 较强的抗肿瘤转移作用，其机制与瘤细胞栓塞、滞留于远隔靶 器官的微血管中并增殖，瘤细胞穿出血管或淋巴管，在靶器 官内形成微转移灶有关。%OBJECTIVE： To study the anti－ metastatic action of equal/unequal－ fork－ peptide of YIGSR.METHODS： To observe the influence of drugs on metastasis of melanoma B16 to lung in mice.RESULTS： The metastatic rate of lung in 46 mice of control and experimental groups was 100％ ,21 days after inoculating melanoma B16 cells via caudal vein.Injection of YIGSR in combination with tumor cells could reduce the number of metastatic nodules in a dose－ dependent manner.The numbers of metastatic nodules in 100μ g～ 200μ g equal fork peptide group and same dosage unequal fork peptide group were significantly different from that in control group(P<0.05;P<0.01 respectively).50μ g equal fork peptide group was different from control group.The synthetic peptide could not decrease the weight of the lung with metastatic lesions.CONCLUSION： YIGSR derivants have effective antimetastatic actions.Its mechanism may related to the inhibiting effect on formation of cancer cell emboli,which retain in microvessels of remote target organs,and multiplicate and penetrate blood vessels to form micrometastatic lesions.