隔药饼灸对动脉粥样硬化兔主动脉内皮细胞PPARγ蛋白及斑块中MMP-9 mRNA表达的影响

Effect of herbal-cake-separated moxibustion on the expression of peroxisome PPAR γ and MMP-9 mRNA in artherosclersis plaques of rabbits

目的:观察隔药饼灸对动脉粥样硬化(AS)兔主动脉内皮细胞中过氧化物酶体增殖物激活受体γ(PPARγ)蛋白及斑块中基质金属蛋白酶-9 mRNA(MMP-9 mRNA)表达的变化,探讨隔药饼灸对兔AS的形成及斑块稳定性的影响。方法:将50只新西兰大耳白兔,通过高脂饲料喂养及免疫损伤法建立兔AS模型,随机分为空白组、模型组、直接灸组、隔药饼灸组和阿托伐他汀组,每组10只,治疗16周后用免疫组化法检测AS兔主动脉内皮细胞中PPARγ的蛋白表达;原位杂交法检测斑块中MMP-9 mRNA的表达。结果:隔药饼灸组、直接灸组和阿托伐他汀组PPARγ的蛋白表达和MMP-9 mRNA的表达均明显低于模型组(P<0.01,P<0.05);隔药饼灸组和阿托伐他汀组动脉粥样硬化斑块中MMP-9 mRNA的表达明显低于直接灸组(P<0.05,P<0.01),隔药饼灸组和阿托伐他汀组比较差异无统计学意义。结论:隔药饼灸可通过激活AS兔主动脉内皮细胞PPARγ的蛋白表达和抑制斑块中MMP-9 mRNA的表达,起到干预AS形成和稳定AS斑块的作用。

Objective： To observe the effect of herbal-cake-separated moxibustion on the expression of peroxisome proliferator-activated receptorγ（PPARγ） and matrix metalloproteinases-9 mRNA（MMP-9 mRNA） in artherosclersis（AS） plaques of rabbits and explore the influence of herbal-cake-separated moxibustion on the formation and stability of As plaque of rabbit.Methods： AS model of rabbit was established by using hypercholesterol diet combined with immunologic injury.50 New Zealand white rabbits were divided into 5 groups： blank group,model group,direct moxibustion group,herbal-cake-separated moxibustion and atorvastatin treated group,10 rabbits per group.The expression of PPARγ in rabbit AS plaque after intervening for 16 weeks was mearsured by immunohistochemical method and the expression of MMP-9 mRNA was determined by hybridization in situ.Results： Compared with the model group,the protein expression of PPARγ and MMP-9 mRNA in herbal-cake-separated moxibustion,direct moxibustion group,and atorvastatin treated group was significantly lower（P0.01,P0.05）.The expression of MMP-9 mRNA in herbal-cake-separated moxibustion and atorvastatin treated group was significantly lower than in diredt moxibustion group（P0.05,P0.01）.There was no significant difference between the atorvastatin treated group and herbal-cake-separated moxibustion.Conclusion： The herbal-cake-separated moxibustion could activate the expression of PPARγ and inhibit the expression of MMP-9 mRNA to intervene the formation and stability of AS plaque.