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[目的]观察四逆汤预干预对高脂血症(HLP)合并动脉粥样硬化(AS)兔的TC、TG、HDL-CH、LDL-CH、Apo-A、Apo-B的影响,分析其对高脂血症(HLP)合并动脉粥样硬化(AS)兔血脂及载脂蛋白的调节作用。[方法]通过高脂饲料喂养及免疫损伤法建立兔HLP合并AS模型,分别给予西药(阿托伐他汀)和四逆汤(高、中、低剂量)的治疗方法。运用酶法测定血中TC、TG含量的变化;比色法测定干预后血中LDL-CH、HDL-CH含量的变化;电泳法测干预后血中载脂蛋白A及B含量的变化。[结果]四逆汤中、高剂量组在降低血TG含量与模型组比具有统计学意义(P<0.05);四逆汤高剂量组在降低血TC、LDL、Apo-B含量与模型组比具有统计学意义(P<0.05);在升高血HDL、Apo-A含量,HDL/LDL比值,Apo-A/Apo-B比值方面,四逆汤高剂量组与模型组比具有显著性差异(P<0.01)。[结论]四逆汤各剂量组均能调节实验性HLP并AS兔血脂代谢,降低胆固醇和甘油三酯的含量,且能降低血中低密度脂蛋白和载脂蛋白B的含量,使其高密度脂蛋白、载脂蛋白A升高。四逆汤预防AS形成的作用机制可能与调节血脂代谢,减缓脂质颗粒沉积有关。
[Objective] To observe the effect of Sini Decoction on TC, TG, HDL-CH, LDL-CH, Apo-A and Apo-B in rabbits with hyperlipidemia (HLP) and atherosclerosis Its regulation of hyperlipemia (HLP) with atherosclerosis (AS) in rabbit serum lipids and apolipoproteins. [Method] Rabbit HLP combined AS model was established by feeding with high fat diet and immunostaining method. The treatment of western medicine (atorvastatin) and Sini decoction (high, medium and low dose) were given respectively. The contents of TC and TG in blood were measured by enzymatic method. The contents of LDL-CH and HDL-CH in blood were determined by colorimetric assay. The levels of apolipoprotein A and B were determined by electrophoresis. [Results] The Sini Decoction medium and high dose groups had statistical significance in reducing blood TG levels compared with the model group (P <0.05). The Sini Decoction high-dose group had the same effect on decreasing the levels of TC, LDL and Apo-B in the model group (P <0.05). Compared with the model group, the high-dose Sini Decoction group had significantly higher serum HDL, Apo-A content, HDL / LDL ratio and Apo-A / Apo-B ratio Difference (P <0.01). [Conclusion] Each dose group of Sini Decoction could regulate the blood lipid metabolism, reduce the content of cholesterol and triglyceride in experimental HLP and AS rabbits, and decrease the content of blood low density lipoprotein and apolipoprotein B Density lipoprotein, apolipoprotein A increased. Sini Decoction to prevent the formation of AS may be related to the mechanism of regulating blood lipid metabolism, slowing the deposition of lipid particles.