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利用ox-LDL对培养的人脐静脉内皮细胞(HUVECs)造成脂质过氧化损伤模型,探讨车前子多糖(PSP)对HUVECs的保护作用及其可能机制。用MTT和化学方法,从细胞水平观察ox-LDL对细胞增殖活性、细胞上清液中一氧化氮(NO)含量、胞内一氧化氮合酶(NOS)活性、丙二醛(MDA)含量、SOD活力;用ELISA和RT-PCR技术,从分子水平观察ICAM-1和凋亡相关基因mRNA的表达,探讨不同浓度的PSP(25 mg/L、50 mg/L、100 mg/L)对上述指标的影响。结果表明ox-LDL导致HUVECs损伤,而伴随PSP浓度的增加,HUVECs增殖活性呈明显升高趋势(P<0.05);而PSP使HUVECsMDA含量显著下降(P<0.05),SOD、NO和NOS水平明显升高(P<0.05),ICAM-1、c-myc mRNA和p53 mRNA表达降低,表明PSP对受损的内皮细胞具有保护作用,其机制可能与抑制ox-LDL诱导的ICAM-1、c-myc mRNA和p53 mRNA的表达有关。
The model of lipid peroxidation induced by ox-LDL on cultured human umbilical vein endothelial cells (HUVECs) was established to investigate the protective effect of psyllium (PSP) on HUVECs and its possible mechanism. The effect of ox-LDL on cell proliferation, the content of nitric oxide (NO), the activity of nitric oxide synthase (NOS) and the content of malondialdehyde (MDA) in cell supernatant were observed by MTT and chemical methods , SOD activity. The expression of ICAM-1 and apoptosis-related gene mRNA were observed by ELISA and RT-PCR at different levels of PSP (25 mg / L, 50 mg / L, 100 mg / L) The impact of the above indicators. The results showed that ox-LDL caused the injury of HUVECs, while the proliferative activity of HUVECs increased with the increase of PSP concentration (P <0.05). However, the content of MDA in HUVECs significantly decreased (P <0.05) (P <0.05), the expression of ICAM-1, c-myc mRNA and p53 mRNA decreased, indicating that PSP could protect the injured endothelial cells. The mechanism may be related to inhibiting the expression of ICAM-1 and c- Myc mRNA and p53 mRNA expression.