摘要
目的 探索SD大鼠胰腺癌组织SST2R及SST2R mRNA的表达以及外源性生长抑素类似物善得定治疗后其表达量的变化。方法 采用二甲基苯丙蒽(DMBA)诱导鼠胰腺癌模型。将实验大鼠随机分为胰腺癌组(A组)、胰腺癌治疗组(B组)、模型制作后未形成胰腺癌的假阳性组(C组),以及正常大鼠组(D组)。在善得定(10μg/kg,每6h1次)治疗前和治疗后的3d、7d、14d,分别取各组胰腺组织标本。分别采用放射免疫法、逆转录聚合酶链法(RT-PCR)分析各组胰腺癌组织SST2R及SST2RmRNA的表达。结果 A、B组SST2R及SST2R mRNA的表达比C、D组显著减少(P<0.05),尤以善得定治疗后的B组减少更为明显,其与A组比较有显著性差异(P<0.05)。B组在治疗后3d、7d、14d时相互比较无显著性差异(P>0.05),但与其治疗前比较有显著性差异(P<0.05)。结论 SD大鼠胰腺癌组织SST2R mRNA和SST2R的表达量明显减少;在善得定治疗后其表达量下降更为明显(P<0.05)。我们认为,胰腺癌组织SST2R mRNA表达量明显减少可能是导致SSTR表达量显著减少和外源性生长抑素类似物治疗临床胰腺癌效果不佳的主要原因之一。
Objective To observe the effect of somatostatin analogues (octreotide) on the expression of protein and mRNA of somatostatin receptor-2(SST2R) in Sprauge Dawley (SD) rats with pancreatic cancer. Methods The rats pancreatic cancer was induced with dimethylbenzanthracine (DMBA). Fifty rats were divided into 4 groups: pancreatic cancer group (group A, rats with pancreatic cancer treated with saline), somatostatin analogues (octreotide, Sandostadin) group (group B, rats with pancreatic cancer treated with Sandostadin), negative control group (group C, rats given DMBA but no pancreatic cancer found), and normal control group (group D). In group A and B, the rats were treated with saline and octeotide (subcutaneous injection, 100 fig, qid) respectively, the protein and mRNA of SST2R in pancreatic cancer tissue were detected by radioimmunoassay or reverse transcription PCR (RT-PCR) 3, 7 and 14 days after treatment. Results The expression of SST2R protein and mRNA decreased significantly in group A and B, especially in group B (P<0.05, vs group C and D). In group B, the expression of SST2R protein and mRNA also decreased significantly after the rats were treated with octreotide (P<0.05, vs pretreatment or group A), but there was no statistic difference 3,7 and 14 days after the octreotide therapy in group B. Conclusions The SST2R protein and mRNA decreased significantly in rat pancreatic cancer tissue. Octreotide can decrease the expression, possibly because of low response of somatostatin analogues in pancreatic cancer.
出处
《胰腺病学》
CAS
2002年第1期41-44,共4页
Chinese JOurnal of Pancreatology
基金
卫生部科研基金(981134)
湖北省自然科学基金(2000J068)