Xu C, Wang X, Wang B, Han S, Zhang Y, Si L
Department of Pathology, Xi'an Medical University, Xi'an 710061, China.
Chin Med J (Engl). 1998 Sep;111(9):861-3.
To investigate the tumor-suppressive activity of polyactin B (PB) and the life-span of tumor bearing mice treated with PB and the anti-tumor mechanisms of PB by blockage of macrophage in vivo.
Thirty-two S180 sarcoma-bearing (s.c.) BALB/c inbred mice were divided into 4 groups, i.e., control group (8 mice), PB group (8), Trypan blue (TrB) group (8) and PB + TrB group (8). Five days after PB injection (i.p.), the tumor size of the mice was measured, and the ratio of TNA to TTA in HE section of the tumor maximal area was calculated and the pathological features of the tumors were observed. Forty S180 sarcoma-bearing (i.p.) ICR mice, which were randomly divided into 4 groups as above, were used for observation of the life-span.
PB could strongly inhibit the growth of S180 sarcoma with the tumors regressing completely in 3 of 8 mice, prolong the life-span of mice bearing S180 sarcoma, increase the infiltration of macrophages and lymphocytes in the periphery and inside of the tumors. In addition, there were more prominent hemorrhagic necrosis, neutrophil infiltration and microthrombi in small vessels around the necrotic areas in the tumors of PB treated group. The tumor-suppressive effect of PB disappeared after macrophage system blockage with TrB. In PB + TrB, TrB, control and PB groups, the size of tumors reduced, and the life-span of mice increased in successive order.
(1) PB is a strong activator of macrophage. (2) In vivo the tumor-suppressive effect of PB is initially mediated by PB activated macrophage system. Then other immunocompetent cells, e.g., T-cells, NK-cells, etc, activated directly and/or indirectly by PB, may play a very important role in tumor suppression. (3) PB-activated macrophages are more sensitive to TrB blockage. Therefore, using TrB + PB to block macrophage system is more effective than TrB alone. (4) Blockage of macrophage function might influence the life-span of the mice.
研究聚肌动蛋白B（PB）的抑瘤活性、PB对荷瘤小鼠生存期的影响以及PB通过体内阻断巨噬细胞发挥的抗肿瘤机制。
将32只皮下接种S180肉瘤的BALB/c近交系小鼠分为4组，即对照组（8只小鼠）、PB组（8只）、台盼蓝（TrB）组（8只）和PB + TrB组（8只）。腹腔注射PB 5天后，测量小鼠肿瘤大小，计算肿瘤最大面积HE切片中肿瘤坏死面积（TNA）与肿瘤总面积（TTA）的比值，并观察肿瘤的病理特征。将40只腹腔接种S180肉瘤的ICR小鼠随机分为上述4组，用于观察生存期。
PB能强烈抑制S180肉瘤的生长，8只小鼠中有3只肿瘤完全消退，可延长荷S180肉瘤小鼠的生存期，增加肿瘤外周及内部巨噬细胞和淋巴细胞的浸润。此外，PB治疗组肿瘤坏死区域周围小血管内出血坏死、中性粒细胞浸润及微血栓更为明显。用TrB阻断巨噬细胞系统后，PB的抑瘤作用消失。在PB + TrB组、TrB组、对照组和PB组中，肿瘤大小依次减小，小鼠生存期依次延长。
（1）PB是巨噬细胞的强激活剂。（2）在体内，PB的抑瘤作用最初由PB激活的巨噬细胞系统介导。随后，由PB直接和/或间接激活的其他免疫活性细胞，如T细胞、NK细胞等，在肿瘤抑制中可能发挥非常重要作用。（3）PB激活的巨噬细胞对TrB阻断更敏感。因此，使用TrB + PB阻断巨噬细胞系统比单独使用TrB更有效。（4）巨噬细胞功能的阻断可能影响小鼠的生存期。
