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目的:探讨力平脂消退动脉粥样硬化的作用机制民。方法:给兔喂饲高脂饲料8周,加腹主动脉内皮损伤造成腹主动脉粥样硬化模型,然后用力平脂15mg·kg~(-1)·d~(-1)治疗16周。粥样硬化血管壁组织中内皮素(ET)-1和一氧化氮合酶(NOS)mRNA的表达分别采用原位杂交和逆转录多聚酶链反应(RT-PCR)测定。结果:力平脂治疗16周后,ET-1 mRNA表达明显减少,其阳性杂交颗粒的积分光密度(IOD)和面积分别由粥样硬化组的(65188±10113)和(3028±352)μm~2下降至(49113±16868)和(2448±621)μm~2。力平脂也可降低诱导型NOS mRNA的表达,使IOD和面积分别下降25.5％和53.3％,但通过RT-PCR测得的内皮型NOS mRNA表达增加。结论:恢复ET-1 mRNA/NOS mRNA的平衡可能是力平脂消退动脉粥样硬化的机制之一。
Objective: To explore the mechanism of action of Lipingzhi on regression of atherosclerosis. Methods: Rabbits were fed with high-fat diet for 8 weeks and abdominal aorta endothelium injury caused by aortic atherosclerosis model, and then the level of lipid 15mg · kg -1 (-1) for 16 weeks. The expression of endothelin (ET) -1 and nitric oxide synthase (NOS) mRNA in atherosclerotic vascular wall tissue were measured by in situ hybridization and reverse transcription polymerase chain reaction (RT-PCR) respectively. Results: After 16 weeks of treatment, the expression level of ET-1 mRNA in LPS-treated mice was significantly decreased, and the IOD and area of positive hybridization particles were (65188 ± 10113) and (3028 ± 352) μm ~ 2 decreased to (49113 ± 16868) and (2448 ± 621) μm ~ 2. Rifalipid also reduced the expression of inducible NOS mRNA and decreased the IOD and area by 25.5% and 53.3%, respectively. However, the expression of endothelial NOS mRNA increased by RT-PCR. CONCLUSION: Restoration of the balance of ET-1 mRNA / NOS mRNA may be one of the mechanisms of atherosclerosis of Lipingzhi.