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目的:通过观察大黄虫丸对小鼠Lewis肺癌细胞黏附因子(CD44)、血管内皮生长因子(VEGF)及转移抑制的影响,初步探讨其抗肿瘤转移的机制。方法:造模后次日先随机分成5组,每组10只。根据预试结果确定高(H)、中(M)、低(S)剂量分别为0.18、0.09、0.045g/ml,以每只0.2ml灌胃10d;空白组小鼠以NS0.2ml灌胃10d;化疗组以50mg/kg CTX于第1d予腹腔给药。第11d处死小鼠,肺玻片压片法观察肺表面的转移灶结节并计数。以免疫组化法检测VEGF的表达;以流式细胞仪测定CD44的活性,初步探讨其抗肿瘤的机制及作用靶点。结果:实验组高(H)、中(M)、低(L)剂量组和化疗组肺自发转移抑制率分别为57.44%、55.32%、38.72%、60.00%。CD44值分别为(0.59±0.86)、(0.21±0.28)、(0.33±0.31)、(1.88±1.36)实验组(M)低于空白组(M)及化疗组(P<0.05)。实验组(M)与空白组比,VEGF阳性表达率明显降低,差异有显著性(P<0.05)。结论:大黄虫丸降低C57BL小鼠Lewis肺癌肺转移发生率,实验组(M)作用明显。实验组(M)还具有抑制C57BL小鼠Lewis肺癌CD44活性,下调C57BL小鼠Lewis肺癌VEGF表达的作用。
OBJECTIVE: To observe the effect of Dahuangqichong Pill on Lewis lung cancer cell adhesion factor (CD44), vascular endothelial growth factor (VEGF) and metastasis inhibition, and to explore its antitumor mechanism. METHODS: The next day after modeling, the rats were randomly divided into 5 groups of 10 in each group. According to the results of the pre-test, high (H), medium (M), and low (S) doses were determined to be 0.18, 0.09, and 0.045 g/ml, respectively, each with 0.2ml gavage for 10 days; the blank group mice were given NS0.2ml gavage 10d; chemotherapy group 50mg/kg CTX on the first day to intraperitoneal administration. On the 11th day, the mice were sacrificed. Lung nodules were observed by lung slides and counted. The expression of VEGF was detected by immunohistochemistry; the activity of CD44 was measured by flow cytometry, and its anti-tumor mechanism and target were initially explored. Results: The inhibitory rate of spontaneous metastasis in the high (H), medium (M), low (L) dose group and chemotherapy group was 57.44%, 55.32%, 38.72%, and 60.00%, respectively. The CD44 values were (0.59±0.86), (0.21±0.28), (0.33±0.31), (1.88±1.36) experimental group (M) lower than the blank group (M) and chemotherapy group (P<0.05). Compared with the blank group, the positive expression rate of VEGF was significantly lower in the experimental group (M) than in the blank group (P<0.05). Conclusion: Dahuangqichong Pill reduces the incidence of lung metastasis of Lewis lung cancer in C57BL mice. The effect of experimental group (M) is obvious. The experimental group (M) also inhibited the CD44 activity of Lewis lung cancer in C57BL mice and down-regulated the expression of VEGF in Lewis lung cancer in C57BL mice.