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本文应用免疫组化,免疫沉淀和点杂交方法研究了血管紧张素Ⅱ(angiotensinⅡ,AⅡ)和δ阿片受体激动剂DPDPE对NG108-15细胞原癌基因c-fos表达的影响。结果表明,10~(-7)mol/L AⅡ可诱导NG108-15细胞c-fos的表达,显著增加Fos样免疫活性(FLI),Fos蛋白含量及c-fos mRNA的表达,这些作用能被特异性AⅡ受体拮抗剂Saralasin拮抗。10~(-7)mol/L DPDPE也能加速NG108-15细胞c-fos的表达,该效应可被阿片受体阻断剂纳洛酮阻断。在等摩尔浓度下,AⅡ的作用显著大于DPDPE。将AⅡ和DPDPE同时作用于细胞,c-fos被诱导表达的水平等于或反而低于AⅡ单独作用时的水平。以上结果首次报道,在神经母细胞和胶质细胞杂交株NG108-15细胞上,激活AⅡ和DPDPE受体均可诱导c-fos原癌基因的表达,而两者同时作用时则有相互抑制效应。
In this study, immunohistochemistry, immunoprecipitation and dot hybridization were used to investigate the effect of angiotensinⅡ (AⅡ) and δ opioid receptor agonist DPDPE on the expression of proto-oncogene c-fos in NG108-15 cells. The results showed that 10 -7 mol / L A Ⅱ could induce c-fos expression in NG108-15 cells, and significantly increased Fos-like immunoreactivity (FLI), Fos protein content and c-fos mRNA expression, these effects could be Specific AII receptor antagonist Saralasin antagonism. 10 ~ (-7) mol / L DPDPE can also accelerate the expression of c-fos in NG108-15 cells, which can be blocked by naloxone, an opioid receptor blocker. At equimolar concentrations, the effect of AII was significantly greater than that of DPDPE. When AⅡ and DPDPE were simultaneously applied to cells, the level of c-fos induced expression was equal to or less than that of AⅡ alone. The above results first reported in the neuroblastoma and glial cell line NG108-15 cells, activation of A Ⅱ and DPDPE receptors can induce the expression of c-fos protooncogene, while the two while having a mutual inhibitory effect .