DDPH对自发性高血压大鼠血管平滑肌细胞增殖及癌基因表达的影响

采用氚－胸腺嘧啶核苷（3H－TdR）参入、电镜、原位杂交及Northern blot杂交方法，观察了 1－ （2，6－二甲基苯氧基）－2－（3，4－二甲氧基苯乙胺基）丙烷盐酸盐（DDPH）对自发性高血压大鼠（SHR）血管平滑肌细胞（VSMC）增殖的作用及对原癌基因及抑癌基因的影响。结果发现：DDPH在降低SHR血压 的同时，能减少VSMC的线粒体、粗面内质网及3H－TdR参入量（P＜0．01），并能逆转c－fos、c－myc、c－sis 原癌基因mRNA表达增强（P＜0．05或＜0．01）以及P53抑癌基因mRNA表达减弱（P＜0．05）。表明： DDPH能抑制SHR的VSMC增殖，与癌基因调控的分子生物学机制有关。

The Effects of DDPH on Proliferation of Vascular Smooth Muscle Cells and Expression of Oncogenes c-myc, c-fos, c-sis and Antioncogene P53 in Spontancously Hypertensive Rat

In order to determine the effects of 1-(2, 6-dimethylphenoxy )-2 -(3, 4-dimethoxyphe-nylethylamino) propane hydrochloride (DDPH) on proliferation of vascular smooth muscle cells (VSMC) and expression of oncogene c-myc, c-fos,c-sis and antioncogene P53 in spontaneously hypertensive rat (SHR),3H-thymidine (3H-TdR ) incorporation, electronic microscopy, in situ hybridization and Northern blot assays were used. The results showed that morphological change of VSMC was antagonized, blood pressure and 3H-TdR data were significantly reduced(P<0. 01 ) after administration of DDPH. Furthermore, DDPH could re-verse the enhanced expression of oncogene c-myc,c-fos,c-sis (P<0.05 or <0.01) and reduced expression of antioncogene P53 (P<0.05) in SHR. These results suggest that DDPH might inhibit DNA synthesis and proliferation of VSMC in SHR, which is related with the mechanism of molecular biology of controlling onco-gene.