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目的:观察化瘀祛痰方药及其拆方对THP-1源性泡沫细胞腺苷三磷酸结合盒转运体A1(ABCA1)、CD36表达的影响,探讨该方药的作用机制,并比较方药全方及各拆方的疗效及调控作用。方法:体外培养THP-1细胞,佛波酯(PMA)使之巨噬化,氧化型低密度脂蛋白(ox-LDL)使巨噬细胞泡沫化。细胞随机分为空白对照组、模型组、补气组、化瘀组、祛痰组和全方组。油红O染色观察细胞浆脂滴变化,酶法测定细胞内总胆固醇(TC)、游离胆固醇(FC)、胆固醇酯(CE)的含量,并计算CE/TC值。反转录-聚合酶链反应(RT-PCR)定量分析ABCA1、CD36 mRNA水平。结果:模型组细胞TC、FC、CE含量及CE/TC值均显著高于对照组(P<0.01);与模型组相比,全方组和祛痰组细胞TC、FC、CE含量及CE/TC值均显著降低。RT-PCR结果提示模型组细胞ABCA1、CD36 mRNA水平显著升高;而化瘀祛痰方药及祛痰拆方含药血清可显著升高ABCA1 mRNA,显著降低CD36 mRNA水平。结论:化瘀祛痰方药及祛痰方可抑制ox-LDL诱导的THP-1细胞泡沫化,该作用可能与其上调ABCA1基因、下调CD36基因表达,从而减弱THP-1细胞对ox-LDL摄取有关。
Objective: To observe the effect of Huatan Qutan Recipe and its decomposed formulas on the expression of ABCA1 and CD36 in THP-1-derived foam cells and to explore the mechanism of action of this prescription and to compare the effects of prescription And the demolition of the curative effect and regulation. METHODS: THP-1 cells were cultured in vitro, macrophages were treated with phorbol myristate (PMA) and ox-LDL to foam macrophages. Cells were randomly divided into blank control group, model group, qi group, Huayu group, expectorant group and the whole group. Oil red O staining was used to observe the change of lipid droplets. The contents of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) were measured by enzyme-linked immunosorbent assay (ELISA) Reverse transcription-polymerase chain reaction (RT-PCR) quantitative analysis of ABCA1, CD36 mRNA levels. Results: The content of TC, FC, CE and the value of CE / TC in the model group were significantly higher than those in the control group (P <0.01). Compared with the model group, the contents of TC, FC, / TC values were significantly lower. The results of RT-PCR indicated that the levels of ABCA1 and CD36 mRNA in the model group were significantly increased. However, the drug-containing serums of Huayu Qutan Recipe and expectorant disassembled serum significantly increased ABCA1 mRNA and significantly decreased the level of CD36 mRNA. Conclusion: Huatan Qutan Recipe and Expectorant Prescription can inhibit ox-LDL-induced foaming of THP-1 cells, which may be related to its up-regulation of ABCA1 gene and down-regulation of CD36 gene expression, thereby reducing the uptake of ox-LDL by THP-1 cells .