论文部分内容阅读
目的:观察通心痹合剂对实验性动脉粥样硬化(atherosclerosis,AS)家兔血脂及炎症细胞因子水平的影响,探讨该方防治AS的机制。方法:将60只家兔随机分为空白组,模型组,辛伐他汀组,通心痹合剂大剂量组、中剂量组、小剂量组,每组10只。以球囊导管内皮损伤术和高脂饵食法建立家兔AS模型,通心痹合剂各剂量组及辛伐他汀组在造模的同时分别给药,空白组、模型组以等量生理盐水灌胃,8周后取出主动脉于光镜下进行病理观察,检测各组大鼠家兔血脂、白细胞介素-6(interleukin-6,IL-6)、IL-1、IL-10、肿瘤坏死因子-α(tumour necrosis factor alpha,TNF-α)。结果:病理结果显示,通心痹合剂大剂量组局部增厚的动脉内膜明显减轻,无泡沫细胞沉积及粥样斑块形成,优于辛伐他汀组;通心痹合剂各剂量组、辛伐他汀组均可明显降低家兔血脂、IL-6、IL-1、TNF-α水平,与模型组比较,差异均有统计学意义(P<0.05,P<0.01),但通心痹合剂大剂量组、中剂量组在降低LDL-C,升高HDL-C、IL-10方面与辛伐他汀组比较,差异有统计学意义(P<0.05,P<0.01)。结论:通心痹合剂对AS有明显的预防和治疗作用,调节血脂和降低炎症细胞因子水平可能是其作用机制之一。
Objective: To observe the effects of Tongxinbi Mixture on serum lipids and inflammatory cytokines in experimental atherosclerosis (AS) rabbits and to explore the mechanism of the prevention and treatment of AS. Methods: Sixty rabbits were randomly divided into blank group, model group, simvastatin group, Tongxinbi Mixture high dose group, medium dose group and low dose group, with 10 rats in each group. The rabbit model of AS was established by balloon catheter endothelial injury and high-fat bait method. Each dose of Tongxinbi Mixture and simvastatin groups were administered separately at the same time. The blank group and model group were treated with normal saline After 8 weeks, the aortas were taken out under the light microscope to observe the pathological changes of blood lipids, interleukin-6 (IL-6), IL-1, IL-10, Tumor necrosis factor alpha (TNF-α). Results: The pathological results showed that Tongxinbi Mixture significantly reduced the local thickening of the intima of the local thickening, the deposition of foam cells and the formation of atherosclerotic plaques were superior to the simvastatin group. Tongxinbi Mixture, Compared with model group, the levels of serum lipids, IL-6, IL-1 and TNF-α in rabbits decreased significantly (all P <0.05, P <0.01) Compared with simvastatin group, the LDL-C, HDL-C and IL-10 levels of high-dose and middle-dose groups were significantly different (P <0.05, P <0.01). Conclusion: Tongxinbi Mixture has obvious preventive and therapeutic effects on AS, and it may be one of its mechanisms of action by regulating blood lipids and decreasing the levels of inflammatory cytokines.