为了探讨 Ephrin－B3在 H22肝癌中的作用及其机制，在野生和 Ephrin－B3敲除基因的 ICR 小鼠上建立 H22肝癌模型，研究 Ephrin－B3在肿瘤生长中的作用。通过称重和 HE 染色考察其对肿瘤的影响，通过电镜观察肿瘤组织细胞结构的改变，通过 Western blot 方法考察其对肿瘤蛋白表达的影响。结果显示：与野生小鼠相比 Ephrin－B3敲除基因小鼠瘤重有非常明显的降低，瘤重分别为（2.45±1.24）g、（1.09±0.56）g，抑制率为55.45％。在形态学观察中，敲除基因小鼠肿瘤组织与野生小鼠相比坏死更严重。在电镜下观察，敲除基因小鼠的肿瘤细胞核中的染色质边缘化较野生小鼠更严重。在蛋白水平上，敲除基因小鼠的 Bax／Bcl－2表达含量明显提高，提示敲除基因后小鼠的肿瘤凋亡增加，从而抑制肿瘤的生长。因此，Ephrin－B3有促进 H22肿瘤生长的作用。%To investigate the inhibiting effects and mechanisms of Ephrin -B3 in liver cancer in vivo,the tumor-bearing mice model was established in the wild-type and Ephrin-B3 knockout mice.The promoting effect was investigated by HE staining.The change of cell morphology and structure was inspected by observ-ing tumor tissue under the electron microscope.The related protein levels were detected by Western blotting. The tumor weight of Ephrin-B3 knockout mice was significantly lower than that of the wild mice.The tumor weight was (2.45±1 .24)g and (1 .09±0.56)g with the inhibition rate of 55.45%.The liver,spleen and thy-mus index were significantly decreased.The necrosis of tumor tissue and the chromatin marginalization of the nucleus in knockout mice were more severe than those in the wild mice.The expression levels of Bax/Bcl-2 were significantly increased in knockout mice.Therefore,Ephrin-B3 had a significant promoting effect on tumor in vivo.
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