中文摘要：

目的：探讨黄芩苷对ApoE基因敲除小鼠早期动脉粥样斑块中基质金属蛋白酶-9（MMP-9）表达的影响。方法：24只8周龄ApoE-/-小鼠均给予高脂饲料喂养8周后随机分为对照组、苷低剂量和高剂量组,每组8只。灌胃8周后处死,酶法检测血清甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）和高密度脂蛋白胆固醇（HDL-C）浓度;用ELISA测血清中MMP-9的表达水平;通过RT-PCR和Western blot检测小鼠主动脉斑块组织中MMP-9的表达情况。结果：与对照组相比,干预组小鼠血清中TC水平降低（P〈0.05）,血清中LDL-C水平明显降低（P〈0.01）,高剂量组较低剂量组降低的明显（P〈0.05）;各组小鼠血清中HDL-C及TG含量虽有变化但无统计学意义。黄芩苷干预组血清MMP-9较对照组表达水平低,高剂量组降低更显著（P〈0.05）;同时,黄芩苷干预组主动脉斑块中MMP-9mRNA及蛋白水平较对照组降低明显（P〈0.01）,高剂量组降低尤为显著（P〈0.05）。结论：黄芩苷可以降低ApoE-/-小鼠血清中血脂和MMP-9水平,并可降低动脉粥样硬化斑块中MMP-9表达,提示黄芩苷具有稳定动脉粥样硬化斑块作用。

英文摘要：

Objective：To explore the effects of Baicalin on the expression of MMP-9at early stage of atherosclerosis in apolipoprotein E knockout mice（ApoE-/-）.Methods：Male 8-week-old ApoE-/-mice fed with high fat diet for 8weeks were randomly divided into three groups（n=8each）：control group,low-dose Baicalin treated group,high-dose Baicalin treated group.All the animals were fed for 8weeks.After administered for 8weeks,mice were sacrificed.serum TG、TC、LDL-C and HDL-C was measured.The serum MMP-9concentration was measured by ELISA.The expression of aortic MMP-9 mRNA and protein in each group mice were determined by Real-time PCR and Western blot respectively.Results：Compared with control group,serum TC level in Baicalin treated groups were reduced（P〈0.05）,serum LDL-C level in Baicalin treated groups were reduced obviously（P〈0.01）,especially in high-dose Baicalin（P 0.05）,but The serum TG、HDL-C level did not have significant differences between groups.The level of serum MMP-9in the Baicalin treated groups was lower than that in the control group,significantly in high-dose Baicalin（P〈0.05）.Meanwhile,the expression of aortic MMP-9mRNA and protein detected by Real-time PCR and Western blot,decreased in Baicalin treated groups compared with that in control group（P 0.01）,which in the high-dose Baicalin treated group were reduced more（P 0.05）.Conclusion：The serum level of Lipids and MMP-9in ApoE-/-mice and the expression of MMP-9in aortic atherosclerotic plaque are reduced by Baicalin,which it shows has regulation function on stability of the plaque.