中国中医药信息杂志
中國中醫藥信息雜誌
중국중의약신식잡지
CHINESE JOURNAL OF INFORMATION ON TRADITIONAL CHINESE MEDICINE
2014年
7期
50-52
,共3页
蔡敏%赵含森%苏毅馨%刘卫红%张蕾%张璐
蔡敏%趙含森%囌毅馨%劉衛紅%張蕾%張璐
채민%조함삼%소의형%류위홍%장뢰%장로
六郁同治%越鞠丸%易损斑块%Ⅰ型胶原%Ⅲ型胶原%基质金属蛋白酶-9%小鼠
六鬱同治%越鞠汍%易損斑塊%Ⅰ型膠原%Ⅲ型膠原%基質金屬蛋白酶-9%小鼠
륙욱동치%월국환%역손반괴%Ⅰ형효원%Ⅲ형효원%기질금속단백매-9%소서
six stagnations elimination therapy%Yueju Wan%vulnerable plaque%typeⅠcollagen%type Ⅲ collagen%metalloproteinase-9%mice
目的:观察六郁同治法对动脉粥样硬化小鼠易损斑块处Ⅰ型、Ⅲ型胶原的含量及基质金属蛋白酶-9(MMP-9)表达的影响,探讨其稳定易损斑块的机制。方法采用高脂饮食喂养ApoE基因敲除小鼠的方法建立易损斑块模型。将小鼠分为正常组、模型组、中药高剂量组、中药低剂量组、辛伐他汀组,每组10只,给药组给予相应药物干预,模型组和正常组给予等量生理盐水,12周后,用苦味酸-天狼星红染色观察Ⅰ型、Ⅲ型胶原,免疫组化法检测MMP-9表达。结果与正常组比较,模型组形成易损斑块;与模型组比较,中药高、低剂量组Ⅰ型胶原增加、Ⅲ型胶原减少(P<0.01),Ⅲ型胶原/Ⅰ型胶原比值降低(P<0.01),MMP-9表达减少(P<0.01)。结论六郁同治法可稳定易损斑块,调节Ⅰ型、Ⅲ胶原的含量和抑制MMP-9的表达可能是其作用机制之一。
目的:觀察六鬱同治法對動脈粥樣硬化小鼠易損斑塊處Ⅰ型、Ⅲ型膠原的含量及基質金屬蛋白酶-9(MMP-9)錶達的影響,探討其穩定易損斑塊的機製。方法採用高脂飲食餵養ApoE基因敲除小鼠的方法建立易損斑塊模型。將小鼠分為正常組、模型組、中藥高劑量組、中藥低劑量組、辛伐他汀組,每組10隻,給藥組給予相應藥物榦預,模型組和正常組給予等量生理鹽水,12週後,用苦味痠-天狼星紅染色觀察Ⅰ型、Ⅲ型膠原,免疫組化法檢測MMP-9錶達。結果與正常組比較,模型組形成易損斑塊;與模型組比較,中藥高、低劑量組Ⅰ型膠原增加、Ⅲ型膠原減少(P<0.01),Ⅲ型膠原/Ⅰ型膠原比值降低(P<0.01),MMP-9錶達減少(P<0.01)。結論六鬱同治法可穩定易損斑塊,調節Ⅰ型、Ⅲ膠原的含量和抑製MMP-9的錶達可能是其作用機製之一。
목적:관찰륙욱동치법대동맥죽양경화소서역손반괴처Ⅰ형、Ⅲ형효원적함량급기질금속단백매-9(MMP-9)표체적영향,탐토기은정역손반괴적궤제。방법채용고지음식위양ApoE기인고제소서적방법건립역손반괴모형。장소서분위정상조、모형조、중약고제량조、중약저제량조、신벌타정조,매조10지,급약조급여상응약물간예,모형조화정상조급여등량생리염수,12주후,용고미산-천랑성홍염색관찰Ⅰ형、Ⅲ형효원,면역조화법검측MMP-9표체。결과여정상조비교,모형조형성역손반괴;여모형조비교,중약고、저제량조Ⅰ형효원증가、Ⅲ형효원감소(P<0.01),Ⅲ형효원/Ⅰ형효원비치강저(P<0.01),MMP-9표체감소(P<0.01)。결론륙욱동치법가은정역손반괴,조절Ⅰ형、Ⅲ효원적함량화억제MMP-9적표체가능시기작용궤제지일。
ObjectiveTo observe the effects of six stagnations elimination therapy on the content of typeⅠ, typeⅢ collagens and matrix metalloproteinase-9 (MMP-9) expression in atherosclerotic mice with vulnerable plaques, to discuss the possible mechanisms of this therapy in stabilizing vulnerable plaques.Methods The ApoE knockout mice were fed on high-fat diets, which built the vulnerable plaques model. Five groups were established, including normal group, model group, high-dose group, low-dose group, and simvastatin group, with 10 mice in each group. Dose groups were given drug intervention, while normal group and model group were given in the same amount of saline. After 12 weeks of drug intervention, the mice were put to death. TypeⅠ and typeⅢcollagens were observed using picric acid-Sirius red staining method. The expression of MMP-9 was detected by immunohistochemical method.ResultsCompared with normal group, vulnerable plaques formed more easily in model group.Compared with model group, typeⅠ collagen increased in high-does and low-dose groups, while typeⅢ collagen, the ratio of typeⅢ andⅠ collagens, and the expression of MMP-9 decreased (P<0.01).ConclusionSix stagnations elimination therapy could stabilize vulnerable plaques. Regulating typeⅠ andⅢ collagens content and inhibiting the expression of MMP-9 may be one of its possible mechanisms.