| 周明学1 徐浩2△ 王绿娅3 刘卫红1 潘琳4.黄连提取物对动脉硬化小鼠斑块胶原类型及MMP-9/TIMP-1 比值
的影响*[J].,2012,12(24):4614-4619 |
| 黄连提取物对动脉硬化小鼠斑块胶原类型及MMP-9/TIMP-1 比值
的影响* |
| Effect of Coptis Root Extract on Collagen category and the Ratio of MMP-9to TIMP-1 in Aortic Vulnerable Atherosclerotic plaque of ApoE-geneKnockout Mice* |
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| DOI： |
| 中文关键词: 黄连提取物 易损斑块 胶原类型 基质金属蛋白酶-9 金属蛋白酶组织抑制剂-1 |
| 英文关键词: Coptis Root Extract Vulnerable atherosclerotic plaque Collagen category Matrix metalloproteinases-9 Tissue inhibitor
of metalloproteinase |
| 基金项目:国家自然科学基金项目（30973702） |
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| 中文摘要: |
| 目的：探讨黄连提取物对高脂喂养ApoE-/- 小鼠主动脉AS 斑块内胶原类型及基质金属蛋白酶-9（MMP-9）与基质金属蛋白
酶组织抑制剂（TIMP-1）比值的影响，探讨黄连提取物稳定斑块的可能作用机制。方法：33 只6-8 周龄的ApoE 基因敲除小鼠予高
脂喂养13 周后，待其形成成熟的AS 斑块后，随机分为3 组：模型组、黄连提取物组、辛伐他汀组（阳性对照组），每组11 只。继续
高脂喂养，并按体重比折算给予小鼠临床推荐剂量的相应药物治疗13 周，处死动物，每只小鼠取主动脉根部的4 个切面，行天狼
猩红染色，检测各组小鼠主动脉斑块内Ⅰ、Ⅲ型胶原含量，以及斑块内MMP-9 和TIMP-1 的表达，计算MMP-9/TIMP-1 比值。结
果：给药13 周后，图像分析结果显示，黄连提取物组小鼠主动脉斑块内Ⅰ型胶原含量与模型组比较有所增加，但无显著差异（P >
0.05）；辛伐他汀组和黄连提取物组小鼠主动脉斑块内Ⅲ型胶原含量与模型组比较显著降低（P<0.01）。Ⅲ型/Ⅰ型胶原比值，两给
药组与模型组比较均显著降低（P<0.01）。与模型组比较，黄连提取物和辛伐他汀组小鼠主动脉斑块内MMP-9 的阳性表达均明显
减少（P<0.01），黄连提取物组主动脉斑块内TIMP-1 的阳性表达与模型组相比明显增加（P<0.01），辛伐他汀组TIMP-1 表达有所
增加，但无统计学差异（P > 0.05），两给药组之间比较无显著差异（P > 0.05）。各给药组中MMP-9/TIMP-1 比值均有所降低，与模型
组比较具有显著差异（P<0.05，P<0.01）。结论：在临床推荐剂量下，黄连提取物可明显改善ApoE-/- 小鼠主动脉AS 斑块内胶原类
型，调整斑块内MMP-9/TIMP-1 比值，从而促进斑块稳定。 |
| 英文摘要: |
| Objective: To observe the effect of Coptis Root Extract (CRE) on collagen category and the ratio of MMP-9 to TIMP-1group was increased but not significantly（P > 0.05）. The difference between the two drug treatment group was not significant（P > 0.05）.
The ratios of MMP-9 to TIMP-1 on the two drug treatment groups were significantly reduced compared with those of the control group
（P<0.05，P<0.01）. Conclusions: In a clinically recommended dose, CRT can significantly modify the collagen category and the ratio of
MMP-9 to TIMP-1 in atherosclerotic plaque of ApoE-gene knockout mice to do favor to plaque stability.
in aortic vulnerable atherosclerotic plaque of high fat fed ApoE-gene knockout mice for exploring the possible mechanism to stabilize
vulnerable plaque. Methods: Thirty-three ApoE-gene knockout mice, 6-8 week age, were fed with high-fat diet for 13 weeks. After mature
atherosclerotic plaque being formed, the animals were randomly allocated into three groups: the control group, the CRE group, the simvastatin
group (as positive control), 11 in each group. They were continuously fed with high-fat diet and the two drug-treated groups,
respective drugs in clinically recommended dose were given for another 13 weeks. Then all mice were sacrificed by the end of experiment.
4 sections of aortic roots in each mouse were examined by Sirius red staining. The contents of typeⅠand Ⅲ collagen and the
expressions of MMP-9 and TIMP-1 in atherosclerotic plaque were detected and their ratios were caculated. Results: After treatment for
13 weeks, compared with that of the control group, the expression of typeⅠcollagen in aortic atherosclerotic plaque in CRE group was
increased but not significant （P > 0.05）, while the expressions of type Ⅲ collagen and the ratio of type Ⅲ to typeⅠcollagen in aortic
atherosclerotic plaque in CRE group and simvastatin group were significantly reduced （P<0.01）. Compared with that of the control
group, the positive expressions of MMP-9 in plaque on CRE group and simvastatin group were significantly reduced （P<0.01）, the expression
of TIMP-1 in plaque on CRE group was significantly increased (P<0.01). The expression of TIMP-1 in plaque on simvastatin |
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