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目的研究十八烯酸对人胃癌移植瘤生长抑制的作用机制。方法取胃癌患者的肿瘤组织,移植到重症联合免疫缺陷(SCID)小鼠上,按照体重将移植胃癌组织的SCID小鼠随机分为3组(每组10只):模型组(腹腔注射等量菜籽油)、对照组(5-氟尿嘧啶:100 mg·kg~(-1))和3个质量分数(十八烯酸:0.2,0.4,0.8g·kg~(-1))实验组,连续4周。用酶联免疫吸附法检测肿瘤组织中环磷酸腺苷(cAMP)、抑癌基因p53(P53)及磷脂酰肌醇-3激酶(P13K)水平。结果低中高3个质量分数实验组和对照组的人胃癌移植瘤生长抑制率分别升高了26.52%,58.75%,67.80%,46.25%,与模型组比较,差异有统计学意义(P<0.01)。这4组人胃癌移植瘤中cAMP水平比模型组分别升高了35.61%,74.93%,130.48%、54.98%,与模型组比较差异有统计学意义(P<0.01)。这4组的人胃癌移植瘤中P53水平比模型组分别降低了57.22%,79.45%,95.71%,80.10%,与模型组比较差异有统计学意义(P<0.01);这4组的的人胃癌移植瘤中P13K水平比模型组分别降低了33.11%,44.39%,97.42%,51.69%,与模型组比较差异有统计学意义(P<0.01)。结论十八烯酸对人胃癌移植瘤生长抑制的作用机制,主要与升高肿瘤组织内cAMP水平、抑制P53和P13K信号通路的活性有关。
Objective To study the mechanism of action of octadecanoic acid on the growth inhibition of human gastric cancer xenografts. Methods Tumor tissues from patients with gastric cancer were transplanted into severe combined immunodeficiency (SCID) mice. SCID mice transplanted with gastric cancer by weight were randomly divided into 3 groups (10 in each group): model group (intraperitoneal injection of equal volume Rapeseed oil), control group (5-fluorouracil: 100 mg · kg -1) and three groups (octadecenoic acid: 0.2,0.4,0.8 g · kg -1) For 4 weeks. The levels of cAMP, P53 and P13K in tumor tissues were detected by enzyme-linked immunosorbent assay (ELISA). Results The growth inhibitory rate of human gastric cancer xenografts increased by 26.52%, 58.75%, 67.80% and 46.25% respectively in experimental group and control group with low, middle and high levels of 3, with significant difference compared with model group (P <0.01) ). Compared with the model group, the levels of cAMP in the 4 groups of gastric cancer transplanted tumors were increased by 35.61%, 74.93%, 130.48% and 54.98%, respectively, which were significantly different from the model group (P <0.01). Compared with the model group, the P53 levels in the 4 groups of human gastric cancer transplanted tumors were reduced by 57.22%, 79.45%, 95.71% and 80.10%, respectively, which were significantly different from those in the model group (P <0.01) The level of P13K in gastric cancer was 33.11%, 44.39%, 97.42% and 51.69% lower than that in the model group, respectively. The difference was statistically significant (P <0.01). Conclusion The mechanism of action of octadecanoic acid on the growth inhibition of human gastric cancer xenografts is mainly related to increasing cAMP level and inhibiting the activity of P53 and P13K signaling pathways.