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目的:观察人参茎叶总皂苷(TG)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的血管平滑肌细胞(VSMCs)增殖的影响及其分子机制。方法:采用四甲基偶氮唑盐(MTT)比色法观察TG对AngⅡ(10-7mol/L)诱导的大鼠VSMC增殖的影响;Real-time-PCR检测VSMC中原癌基因c-fos、c-myc和细胞外信号调节激酶-1(ERK-1)mRNA的表达;Western blotting检测VSMC中丝裂素活化蛋白激酶磷酸酶-1(MKP-1)的表达。结果:AngⅡ明显升高细胞吸光度值(P(0.01),并显著增加c-fos、c-myc、ERK-1 mRNA的表达(P(0.01)。TG(0.05mg/ml,0.1mg/ml)、L-精氨酸(L-arg,0.1mg/ml)均明显抑制AngⅡ诱导的VSMC的增殖,并明显下调AngⅡ所增高的c-fos、c-myc和ERK-1 mRNA的表达(P(0.01)。此外TG还使MKP-1蛋白质表达增强(P<0.05)。结论:TG具有明显的抗血管平滑肌细胞增殖的作用,其机制之一可能与其抑制ERK-1的表达从而抑制原癌基因c-fos、c-myc的表达有关。
OBJECTIVE: To observe the effects of ginsenosides (GS) on the proliferation of vascular smooth muscle cells (VSMCs) induced by angiotensin II (AngII) and its molecular mechanism. METHODS: The effect of TG on the proliferation of rat VSMCs induced by Ang II (10-7 mol/L) was observed by MTT colorimetric assay. The proto-oncogene c-fos in VSMCs was detected by Real-time-PCR. The expression of c-myc and extracellular signal-regulated kinase-1 (ERK-1) mRNA was detected. The expression of mitogen-activated protein kinase phosphatase-1 (MKP-1) in VSMC was detected by Western blotting. RESULTS: AngII significantly increased the cell absorbance (P <0.01) and significantly increased the expression of c-fos, c-myc and ERK-1 mRNA (P <0.01). TG (0.05 mg/ml, 0.1 mg/ml) Both L-arginine (L-arg, 0.1 mg/ml) significantly inhibited the proliferation of VSMCs induced by AngII and significantly down-regulated the expression of c-fos, c-myc and ERK-1 mRNAs (P ( In addition, TG also increased the expression of MKP-1 protein (P<0.05).Conclusion: TG has obvious anti-proliferation effect on vascular smooth muscle cells, and one of the mechanisms may be that it inhibits the expression of ERK-1 and inhibits proto-oncogenes. The expression of c-fos and c-myc is related.