观察卡介苗来源的热休克蛋白HSP65对小鼠移植黑色素瘤的抑制作用并初步探讨可能的作用机制。通过基因工程手段获得纯化的重组HSP65蛋白,与弗氏佐剂联合给药C57BL/6J小鼠。分别设计了两组免疫方案,一组于肿瘤细胞接种前免疫3次,另一组于肿瘤细胞接种前免疫7次。结果在免疫3次的情况下,虽然也能激发较高的特异性抗HSP65抗体,但抑瘤效果不明显(抑瘤率14.2%);增加免疫次数到7次后,抑瘤率高达73.2%,效果显著。经肿瘤组织病理切片发现,增加免疫次数导致肿瘤组织中灶性坏死增加,淋巴细胞浸润增加,且肿瘤细胞病理性核分裂相减少,提示了该疫苗作用的可能机制。
To observe the anti-tumor activity of Mycobacterium tuberculosis Heat Shock Protein 65, the recombination protein HSP65 were expressed in E. coli and purified to mix with Freund' s adjuvant and then immunize two groups of C57BL/6J mice once a week for three times and seven times respectively. Two weeks after last immunization, BI6-F10 melanomas ceils were subcutaneous inoculated to investigate the anti-tumor effect of these vaccines. The results showed that mice immunized HSP65 three times had no significant anti-tumor effect with tumor inhibitory rate of 14.2% while when mice were pretreated with HSP65 seven times, its excised tumors were 73.2% smaller than those from control mice and the pathological section showed more focal necrosis and lymphocyte infiltration while less karyokinesis which implied the possible anti-tumor mechanism. However the precise mechanism still need more investigation.