厚朴酚对高脂饮食诱导的动脉粥样硬化大鼠脂代谢和免疫反应的调节作用

Regulating effect of magnolol on lipid metabolism and immune response in high-fat diet-induced atherosclerotic rats

目的研究厚朴酚对高脂饮食诱导的动脉粥样硬化大鼠脂代谢和免疫反应的影响。方法按照体重将大鼠随机分为5组:正常组、模型组和低、中、高3个剂量实验组,每组10只。高脂饮食诱导动脉粥样硬化大鼠模型。正常组和模型组给予相同体积0. 9%Na Cl;低、中、高3个剂量实验组分别腹腔注射厚朴酚10,20,50 mg·kg^(-1)。以酶联免疫吸附实验检测总胆固醇(TC)、白细胞介素-6 (IL-6)。用流式细胞术检测CD44阳性细胞数。结果正常组、模型组和中、高2个剂量实验组的TC含量分别为(2. 51±0. 44),(9. 42±0. 80),(5. 43±0. 60)和(3. 44±0. 40) mmol·L^(-1);这4组的IL-6含量分别为(6. 06±4. 03),(33. 32±7. 07),(18. 76±8. 78)和(10. 78±4. 24) pg·m L^(-1);这4组的CD44阳性细胞率分别为1. 40±0. 08,23. 51±2. 12,8. 71±1. 52和3. 60±0. 60;上述指标,模型组与正常组比较,差异均有统计学意义(均P <0. 01);中、高2个剂量实验组与模型组相比,差异均有统计学意义(均P <0. 01)。结论厚朴酚可改善高脂饮食诱导的动脉粥样硬化大鼠脂质代谢异常,并减轻炎症反应。

Objective To explore the effect of magnolol on lipid metabolism and immune response in atherosclerotic rats induced by high-fat diet.Methods Rats were randomly divided into 5 groups:normal group,model group,and experimental-L,experimental-M,experimental-H groups,each group had 10 rats.Atherosclerotic rat model was induced by high-fat diet.Normal group and model group were given the same volume of normal saline.The experimental-L,experimental-M,experimental-H groups were given intraperitoneal injection of magnolol(10,20 and 50 mg·kg-1,respectively).The total cholesterol(TC),interleukin-6(IL-6)were detected by enzyme-linked immunosorbent assay.The number of CD44 positive cells was detected by flow cytometry.Results TC contents in normal group,model group and experimental-M,experimental-H groups were respectively(2.51±0.44),(9.42±0.80),(5.43±0.60),(3.44±0.40)mmol·L-1;IL-6 levels in the 4 groups were(6.06±4.03),(33.32±7.07),(18.76±8.78),(10.78±4.24)pg·m L-1;the CD44 positive cells in the 4 groups were 1.40±0.08,23.51±2.12,8.71±1.52,3.60±0.60.Comparison between model group and normal group,the differences of the factors were significant(all P<0.01);comparison between experimental-M,experimental-H groups and model group,the differences of the factors were significant(all P<0.01).Conclusion Magnolol ameliorates the abnormal lipids metabolism and alleviates inflammatory response in atherosclerotic rats induced by high-fat diet.