摘要
目的探讨马齿苋脂肪油有效成分对肝脏卵磷脂胆固醇酯酰转移酶(LCAT)、载脂蛋白AI(apoAI)和高密度脂蛋白受体(SR-BI)基因表达的干预作用,分析马齿苋调节胆固醇逆向转运(RCT)通路的分子机制。方法健康雄性SD大鼠24只,随机分为模型组、多烯康组、马齿苋组、正常组,每组6只。应用高脂高胆固醇膳食诱导建立动脉粥样硬化(AS)大鼠模型,用定量反转录聚合酶链式反应(RT-PCR)技术测定LCAT、apoAI及SR-BI mRNA表达量,以免疫比浊法、沉淀法测定血清apoAI、高密度脂蛋白胆固醇(HDL-C)含量。结果模型组大鼠肝脏LCAT mRNA和apoAI mRNA的表达量明显下降,分别为0.43±0.20、2.33±0.35,与正常组(分别为1.49±0.32、6.30±0.82)、多烯康组(分别为1.15±0.16、4.32±0.69)、马齿苋组(分别为1.12±0.12、4.21±0.76)比较,差异均有统计学意义(P<0.05)。模型组大鼠血清apoAI([0.15±0.03)g/L]和HDL-C水平([0.53±0.25)mmol/L]明显下降,与马齿苋组([0.39±0.09)g/L、(0.86±0.04)mmol/L]比较,差异有统计学意义(P<0.05)。除正常组外,多烯康组、马齿苋组、模型组肝脏LCAT mRNA表达量与HDL-C水平均呈明显的正相关(r值分别为0.935、0.927、0.892,P<0.01)。模型组大鼠肝脏SR-BI mRNA水平(1.33±0.57)下降,马齿苋组(3.20±0.41)高于模型组,差异有统计学意义(P<0.01)。结论在转录水平阻抗高脂高胆固醇负荷下调大鼠肝脏LCAT和apoAI mRNA以及SR-BI mRNA表达的作用,促进RCT过程是马齿苋改善高脂血症、抗动脉粥样硬化的重要分子机制。
Objective To explore the effects of portulaca oleracea fatty oil active ingredients on hepatic lecithin cholesterol acyl transferase （LCAT）, apolipoproteinAI （apoAI） and high density lipoprotein receptor（SR-BI） gene expression and to analyze the molecular mechanism of regulating reverse cholesterol transportation（RCT） pathway by purslane. Methods Twenty four healthy male SD rats were randomly divided into four groups： model group, duoxikang group, portulaca group and the control group （6 rats each group）. Animal model of atherosclerosis （AS） was prepared with high-fat and high-cholesterol diet. RT-PCR was used to detect the expression levels of hepatic LCAT, apoAI and SR-BI mRNA. The serum apoAI and HDL-C levels were measured with immune turbidimetry and precipitation methods. Results The expression levels of hepatic LCAT mRNA and apoAI mRNA in model group were 0.43±0.20 and 2.33±0.35 respectively, which were significantly lower than those （ 1.49±0.32 and 6.30±0.82） in control group, those （1.15±0.16 and 4.32±0.69） in duoxikang group and those （ 1.12±0.12 and 4.21±0.76） in portulaca group （P〈0.05）. The serum apoAI and HDL-C levels in model group were （0.15±0.03） g/L and （0.53±0.25） mmol/L respectively, which were significantly lower than those [（0.39±0.09） g/L and （0.86±0.04） retool/L] in portulaca group （P〈0.05）. There were positive correlation between hepatic expression levels and serum HDL-C levels in duoxikang group, portulaca group and model group （r=0.935, 0.927 and 0.892,P〈0.01 ）. The hepatic SR-BI mRNA expression level （1.33±0.57） in model group was obviously lower than that （3.20±0.41） in portulaca group （P〈0.05）. Conclusion The molecular mechanisms of purslane anti-AS effects may be due to own-regulating hepatic LCAT, apoAI and SR-BI mRNA expression and improving RCT.
出处
《中国慢性病预防与控制》
CAS
2013年第1期12-14,共3页
Chinese Journal of Prevention and Control of Chronic Diseases
基金
山东省科技厅资助课题(2006GG2302015)
山东省中医药管理局资助课题(2005236)
关键词
动脉粥样硬化
马齿苋
载脂蛋白
基因表达
卵磷脂胆固醇酯酰转移酶
高密度脂蛋白受体
胆固醇逆向转运
Atherosclerosis
Purslane
Apolipoprotein
Gene expression
Lecithin cholesterol acyl transferase
High density lipoprotein receptor
Reverses cholesterol transportation
